Yusha Zhu - New York University (original) (raw)

Papers by Yusha Zhu

Role of miR-31 and SATB2 in arsenic-induced malignant BEAS-2B cell transformation

Molecular Carcinogenesis, Apr 17, 2018

Arsenic is a naturally occurring and highly potent metalloid known to elicit serious public healt... more Arsenic is a naturally occurring and highly potent metalloid known to elicit serious public health concerns. Today, approximately 200 million people around the globe are exposed to arsenic-contaminated drinking water at levels greater than the World Health Organization's recommended limit of 10 parts per billion. As a class I human carcinogen, arsenic exposure is known to elicit various cancers, including lung, skin, liver, and kidney. Current evidence suggests that arsenic is capable of inducing both genotoxic and cytotoxic injury, as well as activating epigenetic pathways to induce carcinogenesis. Our study identifies a novel pathway that is implicated in arsenic-induced carcinogenesis. Arsenic down-regulated miRNA-31 and the release of this inhibition caused overexpression of special AT-rich sequence-binding protein 2 (SATB2). Arsenic is known to disrupt miRNA expression, and here we report for the first time that arsenic is capable of inhibiting miR-31 expression. As a direct downstream target of miR-31, SATB2 is a prominent transcription factor, and nuclear matrix binding protein implicated in many types of human diseases including lung cancer. Results from this study show that arsenic induces the overexpressing SATB2 by inhibiting miR-31 expression, which blocks the translation of SATB2 mRNA, since levels of SATB2 mRNA remain the same but protein levels decrease. Overexpression of SATB2 induces malignant transformation of human bronchial epithelial (BEAS-2B) cells indicating the importance of the expression of miR-31 in preventing carcinogenesis by suppressing SATB2 protein levels.

Wrong place, wrong time: Runt-related transcription factor 2/SATB2 pathway in bone development and carcinogenesis

Journal of Carcinogenesis, 2021

Upregulation or aberrant expression of genes such as special AT-rich sequence-binding protein 2 (... more Upregulation or aberrant expression of genes such as special AT-rich sequence-binding protein 2 (SATB2) is necessary for normal cell differentiation and tissue development and is often associated with carcinogenesis and metastatic progression. SATB2 is a critical transcription factor for biological development of various specialized cell lineages, such as osteoblasts and neurons. The dysregulation of SATB2 expression has recently been associated with various types of cancer, while the mechanisms and pathways by which it mediates tumorigenesis are not well elucidated. Runt-related transcription factor 2 (RUNX2) is a master regulator for osteogenesis, and it shares common pathways with SATB2 to regulate bone development. Interestingly, these two transcription factors co-occur in several epithelial and mesenchymal cancers and are linked by multiple cancer-related proteins and microRNAs. This review examines the interactions between RUNX2 and SATB2 in a network necessary for normal bone...

RUNX2/miR‑31/SATB2 pathway in nickel‑induced BEAS‑2B cell transformation

Nickel (Ni) compounds are classified as Group 1 carcinogens by the International Agency for Resea... more Nickel (Ni) compounds are classified as Group 1 carcinogens by the International Agency for Research on Cancer (IARC) and are known to be carcinogenic to the lungs. In our previous study, special AT‑rich sequence‑binding protein 2 (SATB2) was required for Ni‑induced BEAS‑2B cell transformation. In the present study, a pathway that regulates the expression of SATB2 protein was investigated in Ni‑transformed BEAS‑2B cells using western blotting and RT‑qPCR for expression, and soft agar, migration and invasion assays for cell transformation. Runt‑related transcription factor 2 (RUNX2), a master regulator of osteogenesis and an oncogene, was identified as an upstream regulator for SATB2. Ni induced RUNX2 expression and initiated BEAS‑2B transformation and metastatic potential. Previously, miRNA‑31 was identified as a negative regulator of SATB2 during arsenic‑induced cell transformation, and in the present study it was identified as a downstream target of RUNX2 during carcinogenesis. mi...

Metals and Molecular Carcinogenesis

Carcinogenesis, 2020

Many metals are essential for living organisms, but at higher doses they may be toxic and carcino... more Many metals are essential for living organisms, but at higher doses they may be toxic and carcinogenic. Metal exposure occurs mainly in occupational settings and environmental contaminations in drinking water, air pollution and foods, which can result in serious health problems such as cancer. Arsenic (As), Beryllium (Be), Cadmium (Cd), Chromium (Cr), and Nickel (Ni) are classified as Group 1 carcinogens by the International Agency for Research on Cancer. This review provides a comprehensive summary of current concepts of the molecular mechanisms of metal-induced carcinogenesis and focusing on a variety of pathways, including genotoxicity, mutagenesis, oxidative stress, epigenetic modifications such as DNA methylation, histone posttranslational modification and alteration in miRNA regulation, competition with essential metal ions, and cancer-related signalling pathways. This review takes a broader perspective and aims to assist in guiding future research with respect to the preventi...

SSRN Electronic Journal, 2019

Polyadenylation of canonical histone H3.1 mRNA promotes tumor formation in nude mice • Histone va... more Polyadenylation of canonical histone H3.1 mRNA promotes tumor formation in nude mice • Histone variant H3.3 is displaced from critical gene regulatory elements by overexpression of polyadenylated H3.1 mRNA • Increased polyadenylated H3.1 mRNA causes abnormal transcription, cell cycle arrest, and chromosomal instability • Arsenic induces polyadenylation of H3.1 mRNA in vivo

Inorganics, Jun 28, 2019

Nickel is a naturally occurring element found in the Earth's crust and an International Agency fo... more Nickel is a naturally occurring element found in the Earth's crust and an International Agency for Research on Cancer (IARC)-classified human carcinogen. While low levels found in the natural environment pose a minor concern, the extensive use of nickel in industrial settings such as in the production of stainless steel and various alloys complicate human exposure and health effects. Notably, interactions with nickel macromolecules, primarily through inhalation, have been demonstrated to promote lung cancer. Mechanisms of nickel-carcinogenesis range from oxidative stress, DNA damage, and hypoxia-inducible pathways to epigenetic mechanisms. Recently, non-coding RNAs have drawn increased attention in cancer mechanistic studies. Specifically, nickel has been found to disrupt expression and functions of micro-RNAs and long-non-coding RNAs, resulting in subsequent changes in target gene expression levels, some of which include key cancer genes such as p53, MDM2, c-myc, and AP-1. Non-coding RNAs are also involved in well-studied mechanisms of nickel-induced lung carcinogenesis, such as the hypoxia-inducible factor (HIF) pathway, oxidative stress, DNA damage and repair, DNA hypermethylation, and alterations in tumor suppressors and oncogenes. This review provides a summary of the currently known epigenetic mechanisms involved in nickel-induced lung carcinogenesis, with a particular focus on non-coding RNAs.

Abstract 4403: Regulation of SATB2 via miR-31 in Ni-induced malignant cell transformation

Molecular and Cellular Biology / Genetics

The special AT-rich DNA binding protein (SATB2) is a nuclear matrix associated protein and an imp... more The special AT-rich DNA binding protein (SATB2) is a nuclear matrix associated protein and an important transcription factor for biological development, gene regulation, and chromatin remodeling. Under normal circumstances, SATB2 is not expressed in most cells, including epithelial cells of the lung. However, aberrant regulation of SATB2 has been found in various types of cancers including lung, colon, prostate, breast, gastric, and liver. Emerging studies have linked the possible role of SATB2 in carcinogenic metal-induced cell transformation. In fact, our previous microarray analysis showed that SATB2 is strongly induced in Ni-transformed cells. As an IARC Class I Human Carcinogen, there is well-established link between chronic nickel exposure and lung cancer; however, despite of considerable research efforts in regards to the epigenetic mechanisms, little is known about the role of microRNAs in Ni-induced carcinogenesis. As post-transcriptional regulators, miRNAs have great importance in maintaining normal cellular development. In particular, miR-31 is one of the most abundant types of miRNAs and commonly studied in disease development, including cancers of the lung, breast, and liver. Previous studies have shown the miR-31 can directly target the homeobox gene SATB, and here we report that miR-31 is capable of regulating SATB2 in Ni-induced tumorigenesis. First, our results confirmed that knocking down SATB2 in Ni-transformed BEAS-2B cells via shRNA significantly reduced the rate of migration, anchorage-independent growth. Notably, compared to scramble control shRNA transfected cells, SATB2 knockdown cells did not generate tumor growth in mice xenograft model. These results highlight the oncogenic role of SATB2 in cell transformation. In addition, our data indicate that both acute Ni-treated and Ni-transformed cells demonstrated significant reduction in miR-31 expression. Furthermore, we show that overexpressing miR-31 in Ni-transformed cells reduced rates of migration, anchorage-independent growth, and cellular invasion, indicating the importance of miR-31 in Ni-induced BEAS-2B cell transformation. Together, our results provide a novel mechanistic pathway for Ni-induced carcinogenesis, and add to the pool of existing research on the implications of SATB2 and miR-31 in tumorigenesis. Citation Format: Qiao Yi Chen, Yusha Zhu, Ashley Jordan, Jinquan Li, Hong Sun, Thomas Kluz, Max Costa. Regulation of SATB2 via miR-31 in Ni-induced malignant cell transformation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 4403.

Abstract 1480: Overexpression of histone H3.1 induced cell malignant transformation and mutation of H3.1 C96/110A further induced chromatin instability

Molecular and Cellular Biology / Genetics

Histones are major proteins in chromatin and are important for chromatin structure and gene expre... more Histones are major proteins in chromatin and are important for chromatin structure and gene expression. Canonical histones are defined as a group of replication-dependent histone proteins and are mainly synthesized during S phase of the cell cycle. Their mRNAs are devoid of poly-adenylated tails, but end up with a stem loop structure, which can be targeted by proteins such as stem-loop binding proteins (SLBP) for processing, exportation, and degradation. In our previous studies, arsenic exposure was found to be associated with reduced levels of SLBP and accumulation of poly-adenylated mRNA of canonical histone H3.1, and ultimately led to malignant transformation of cells. Histone H3.1 and H3.2 are canonical histones and they differ by only one amino acid, Ser96 on H3.2 compared with Cys96 on H3.1, and both of them have a Cys110. Histone H3 is the only histone that contains cysteine. Cysteine (C) is a unique amino acid that is rarely used by nature and it has a reactive thiol side chain that can easily form dimers containing disulfide bridge when oxidized. Here it is hypothesized that cysteine is vital for the structure and stability of chromatin. To test this hypothesis, we generated an H3.1 mutant H3.1 C96/110A, where two cysteine residues were replaced by alanine (A). The wild-type H3.1 and H3.1 C96/110A were exogenously expressed in the Beas-2B cells. Interestingly, Beas-2B cells ectopically expressing poly-adenylated H3.1 and H3.1 C96/110A showed decreased proliferation rate with cell cycle arrest at S phase, and cells also acquired cancer cell properties such as increased anchorage-independent growth along with migration and invasion ability. It was confirmed that H3.1 C96/110A could be incorporated into chromatin, resulting in increased chromatin instability and DNA damage. In addition, the RNA-seq assay revealed a total of 678 genes that were oppositely expressed between H3.1 and H3.1 C96/110A ectopically expressed cells. These findings emphasize the importance of a balance among histone variants in the cell and an essential role of cysteines in histone H3.1. Citation Format: Yusha Zhu, Hong Sun, Max Costa. Overexpression of histone H3.1 induced cell malignant transformation and mutation of H3.1 C96/110A further induced chromatin instability [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1480.

Abstract 5857: Isorhapontigenin inhibits triple-negative breast cancer via activating NRF2-mediated pathway

Cancer Research, 2018

Breast cancer is the most prevalent cancer among women worldwide, and is the second leading cause... more Breast cancer is the most prevalent cancer among women worldwide, and is the second leading cause of cancer mortality among women. Triple-negative breast cancers (TNBCs; ER-/PR-/HER2-) are highly aggressive tumors with poor prognosis. Due to lack of these specific receptors, TNBCs cannot be treated with hormone therapies or anti-HER2 targeted therapies. Chemotherapy, combined with surgery and radiation therapy, is the primary strategy for treating TNBCs. Thus, discovery and evaluation of new alternative medications targeting triple-negative breast cancer is of tremendous importance for reducing breast cancer mortality. Isorhapontigenin (ISO), a new derivative of stilbene isolated from Chinese herb Gnetum Cleistostachyun, exhibits a strong inhibitory effect on human bladder cancers. However, its anticancer activity with respect to breast cancer remains unclear. In the present study, we investigated the potential anticancer effect of ISO on TNBCs. ISO treatment inhibited the prolifera...

Abstract 356: Polyadenyaltion of canonical histone mRNA: A potential mechanism of arsenic-induced carcinogenesis

Molecular and Cellular Biology / Genetics

Role of miR-31 and SATB2 in arsenic-induced malignant BEAS-2B cell transformation

Molecular Carcinogenesis, Apr 17, 2018

Arsenic is a naturally occurring and highly potent metalloid known to elicit serious public healt... more Arsenic is a naturally occurring and highly potent metalloid known to elicit serious public health concerns. Today, approximately 200 million people around the globe are exposed to arsenic-contaminated drinking water at levels greater than the World Health Organization's recommended limit of 10 parts per billion. As a class I human carcinogen, arsenic exposure is known to elicit various cancers, including lung, skin, liver, and kidney. Current evidence suggests that arsenic is capable of inducing both genotoxic and cytotoxic injury, as well as activating epigenetic pathways to induce carcinogenesis. Our study identifies a novel pathway that is implicated in arsenic-induced carcinogenesis. Arsenic down-regulated miRNA-31 and the release of this inhibition caused overexpression of special AT-rich sequence-binding protein 2 (SATB2). Arsenic is known to disrupt miRNA expression, and here we report for the first time that arsenic is capable of inhibiting miR-31 expression. As a direct downstream target of miR-31, SATB2 is a prominent transcription factor, and nuclear matrix binding protein implicated in many types of human diseases including lung cancer. Results from this study show that arsenic induces the overexpressing SATB2 by inhibiting miR-31 expression, which blocks the translation of SATB2 mRNA, since levels of SATB2 mRNA remain the same but protein levels decrease. Overexpression of SATB2 induces malignant transformation of human bronchial epithelial (BEAS-2B) cells indicating the importance of the expression of miR-31 in preventing carcinogenesis by suppressing SATB2 protein levels.

Wrong place, wrong time: Runt-related transcription factor 2/SATB2 pathway in bone development and carcinogenesis

Journal of Carcinogenesis, 2021

Upregulation or aberrant expression of genes such as special AT-rich sequence-binding protein 2 (... more Upregulation or aberrant expression of genes such as special AT-rich sequence-binding protein 2 (SATB2) is necessary for normal cell differentiation and tissue development and is often associated with carcinogenesis and metastatic progression. SATB2 is a critical transcription factor for biological development of various specialized cell lineages, such as osteoblasts and neurons. The dysregulation of SATB2 expression has recently been associated with various types of cancer, while the mechanisms and pathways by which it mediates tumorigenesis are not well elucidated. Runt-related transcription factor 2 (RUNX2) is a master regulator for osteogenesis, and it shares common pathways with SATB2 to regulate bone development. Interestingly, these two transcription factors co-occur in several epithelial and mesenchymal cancers and are linked by multiple cancer-related proteins and microRNAs. This review examines the interactions between RUNX2 and SATB2 in a network necessary for normal bone...

RUNX2/miR‑31/SATB2 pathway in nickel‑induced BEAS‑2B cell transformation

Nickel (Ni) compounds are classified as Group 1 carcinogens by the International Agency for Resea... more Nickel (Ni) compounds are classified as Group 1 carcinogens by the International Agency for Research on Cancer (IARC) and are known to be carcinogenic to the lungs. In our previous study, special AT‑rich sequence‑binding protein 2 (SATB2) was required for Ni‑induced BEAS‑2B cell transformation. In the present study, a pathway that regulates the expression of SATB2 protein was investigated in Ni‑transformed BEAS‑2B cells using western blotting and RT‑qPCR for expression, and soft agar, migration and invasion assays for cell transformation. Runt‑related transcription factor 2 (RUNX2), a master regulator of osteogenesis and an oncogene, was identified as an upstream regulator for SATB2. Ni induced RUNX2 expression and initiated BEAS‑2B transformation and metastatic potential. Previously, miRNA‑31 was identified as a negative regulator of SATB2 during arsenic‑induced cell transformation, and in the present study it was identified as a downstream target of RUNX2 during carcinogenesis. mi...

Metals and Molecular Carcinogenesis

Carcinogenesis, 2020

Many metals are essential for living organisms, but at higher doses they may be toxic and carcino... more Many metals are essential for living organisms, but at higher doses they may be toxic and carcinogenic. Metal exposure occurs mainly in occupational settings and environmental contaminations in drinking water, air pollution and foods, which can result in serious health problems such as cancer. Arsenic (As), Beryllium (Be), Cadmium (Cd), Chromium (Cr), and Nickel (Ni) are classified as Group 1 carcinogens by the International Agency for Research on Cancer. This review provides a comprehensive summary of current concepts of the molecular mechanisms of metal-induced carcinogenesis and focusing on a variety of pathways, including genotoxicity, mutagenesis, oxidative stress, epigenetic modifications such as DNA methylation, histone posttranslational modification and alteration in miRNA regulation, competition with essential metal ions, and cancer-related signalling pathways. This review takes a broader perspective and aims to assist in guiding future research with respect to the preventi...

SSRN Electronic Journal, 2019

Polyadenylation of canonical histone H3.1 mRNA promotes tumor formation in nude mice • Histone va... more Polyadenylation of canonical histone H3.1 mRNA promotes tumor formation in nude mice • Histone variant H3.3 is displaced from critical gene regulatory elements by overexpression of polyadenylated H3.1 mRNA • Increased polyadenylated H3.1 mRNA causes abnormal transcription, cell cycle arrest, and chromosomal instability • Arsenic induces polyadenylation of H3.1 mRNA in vivo

Inorganics, Jun 28, 2019

Nickel is a naturally occurring element found in the Earth's crust and an International Agency fo... more Nickel is a naturally occurring element found in the Earth's crust and an International Agency for Research on Cancer (IARC)-classified human carcinogen. While low levels found in the natural environment pose a minor concern, the extensive use of nickel in industrial settings such as in the production of stainless steel and various alloys complicate human exposure and health effects. Notably, interactions with nickel macromolecules, primarily through inhalation, have been demonstrated to promote lung cancer. Mechanisms of nickel-carcinogenesis range from oxidative stress, DNA damage, and hypoxia-inducible pathways to epigenetic mechanisms. Recently, non-coding RNAs have drawn increased attention in cancer mechanistic studies. Specifically, nickel has been found to disrupt expression and functions of micro-RNAs and long-non-coding RNAs, resulting in subsequent changes in target gene expression levels, some of which include key cancer genes such as p53, MDM2, c-myc, and AP-1. Non-coding RNAs are also involved in well-studied mechanisms of nickel-induced lung carcinogenesis, such as the hypoxia-inducible factor (HIF) pathway, oxidative stress, DNA damage and repair, DNA hypermethylation, and alterations in tumor suppressors and oncogenes. This review provides a summary of the currently known epigenetic mechanisms involved in nickel-induced lung carcinogenesis, with a particular focus on non-coding RNAs.

Abstract 4403: Regulation of SATB2 via miR-31 in Ni-induced malignant cell transformation

Molecular and Cellular Biology / Genetics

The special AT-rich DNA binding protein (SATB2) is a nuclear matrix associated protein and an imp... more The special AT-rich DNA binding protein (SATB2) is a nuclear matrix associated protein and an important transcription factor for biological development, gene regulation, and chromatin remodeling. Under normal circumstances, SATB2 is not expressed in most cells, including epithelial cells of the lung. However, aberrant regulation of SATB2 has been found in various types of cancers including lung, colon, prostate, breast, gastric, and liver. Emerging studies have linked the possible role of SATB2 in carcinogenic metal-induced cell transformation. In fact, our previous microarray analysis showed that SATB2 is strongly induced in Ni-transformed cells. As an IARC Class I Human Carcinogen, there is well-established link between chronic nickel exposure and lung cancer; however, despite of considerable research efforts in regards to the epigenetic mechanisms, little is known about the role of microRNAs in Ni-induced carcinogenesis. As post-transcriptional regulators, miRNAs have great importance in maintaining normal cellular development. In particular, miR-31 is one of the most abundant types of miRNAs and commonly studied in disease development, including cancers of the lung, breast, and liver. Previous studies have shown the miR-31 can directly target the homeobox gene SATB, and here we report that miR-31 is capable of regulating SATB2 in Ni-induced tumorigenesis. First, our results confirmed that knocking down SATB2 in Ni-transformed BEAS-2B cells via shRNA significantly reduced the rate of migration, anchorage-independent growth. Notably, compared to scramble control shRNA transfected cells, SATB2 knockdown cells did not generate tumor growth in mice xenograft model. These results highlight the oncogenic role of SATB2 in cell transformation. In addition, our data indicate that both acute Ni-treated and Ni-transformed cells demonstrated significant reduction in miR-31 expression. Furthermore, we show that overexpressing miR-31 in Ni-transformed cells reduced rates of migration, anchorage-independent growth, and cellular invasion, indicating the importance of miR-31 in Ni-induced BEAS-2B cell transformation. Together, our results provide a novel mechanistic pathway for Ni-induced carcinogenesis, and add to the pool of existing research on the implications of SATB2 and miR-31 in tumorigenesis. Citation Format: Qiao Yi Chen, Yusha Zhu, Ashley Jordan, Jinquan Li, Hong Sun, Thomas Kluz, Max Costa. Regulation of SATB2 via miR-31 in Ni-induced malignant cell transformation [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 4403.

Abstract 1480: Overexpression of histone H3.1 induced cell malignant transformation and mutation of H3.1 C96/110A further induced chromatin instability

Molecular and Cellular Biology / Genetics

Histones are major proteins in chromatin and are important for chromatin structure and gene expre... more Histones are major proteins in chromatin and are important for chromatin structure and gene expression. Canonical histones are defined as a group of replication-dependent histone proteins and are mainly synthesized during S phase of the cell cycle. Their mRNAs are devoid of poly-adenylated tails, but end up with a stem loop structure, which can be targeted by proteins such as stem-loop binding proteins (SLBP) for processing, exportation, and degradation. In our previous studies, arsenic exposure was found to be associated with reduced levels of SLBP and accumulation of poly-adenylated mRNA of canonical histone H3.1, and ultimately led to malignant transformation of cells. Histone H3.1 and H3.2 are canonical histones and they differ by only one amino acid, Ser96 on H3.2 compared with Cys96 on H3.1, and both of them have a Cys110. Histone H3 is the only histone that contains cysteine. Cysteine (C) is a unique amino acid that is rarely used by nature and it has a reactive thiol side chain that can easily form dimers containing disulfide bridge when oxidized. Here it is hypothesized that cysteine is vital for the structure and stability of chromatin. To test this hypothesis, we generated an H3.1 mutant H3.1 C96/110A, where two cysteine residues were replaced by alanine (A). The wild-type H3.1 and H3.1 C96/110A were exogenously expressed in the Beas-2B cells. Interestingly, Beas-2B cells ectopically expressing poly-adenylated H3.1 and H3.1 C96/110A showed decreased proliferation rate with cell cycle arrest at S phase, and cells also acquired cancer cell properties such as increased anchorage-independent growth along with migration and invasion ability. It was confirmed that H3.1 C96/110A could be incorporated into chromatin, resulting in increased chromatin instability and DNA damage. In addition, the RNA-seq assay revealed a total of 678 genes that were oppositely expressed between H3.1 and H3.1 C96/110A ectopically expressed cells. These findings emphasize the importance of a balance among histone variants in the cell and an essential role of cysteines in histone H3.1. Citation Format: Yusha Zhu, Hong Sun, Max Costa. Overexpression of histone H3.1 induced cell malignant transformation and mutation of H3.1 C96/110A further induced chromatin instability [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 1480.

Abstract 5857: Isorhapontigenin inhibits triple-negative breast cancer via activating NRF2-mediated pathway

Cancer Research, 2018

Breast cancer is the most prevalent cancer among women worldwide, and is the second leading cause... more Breast cancer is the most prevalent cancer among women worldwide, and is the second leading cause of cancer mortality among women. Triple-negative breast cancers (TNBCs; ER-/PR-/HER2-) are highly aggressive tumors with poor prognosis. Due to lack of these specific receptors, TNBCs cannot be treated with hormone therapies or anti-HER2 targeted therapies. Chemotherapy, combined with surgery and radiation therapy, is the primary strategy for treating TNBCs. Thus, discovery and evaluation of new alternative medications targeting triple-negative breast cancer is of tremendous importance for reducing breast cancer mortality. Isorhapontigenin (ISO), a new derivative of stilbene isolated from Chinese herb Gnetum Cleistostachyun, exhibits a strong inhibitory effect on human bladder cancers. However, its anticancer activity with respect to breast cancer remains unclear. In the present study, we investigated the potential anticancer effect of ISO on TNBCs. ISO treatment inhibited the prolifera...

Abstract 356: Polyadenyaltion of canonical histone mRNA: A potential mechanism of arsenic-induced carcinogenesis

Molecular and Cellular Biology / Genetics