Anissa SARI - Academia.edu (original) (raw)

Papers by Anissa SARI

Research paper thumbnail of BIO-MASTIC (Mastitis Natural Antiseptic), Pemanfaatan Ekstrak Daun Kersen sebagai Antiseptik Tear Dipping

"BIO-MASTIC" is based natural antiseptic compounds containing antibacterial protection ... more "BIO-MASTIC" is based natural antiseptic compounds containing antibacterial protection cherry leaves. thing more support in making this antiseptic is a special antiseptic product innovation Teat Dipping that has never existed in the market, another advantage with natural ingredients that have been tested, so as to provide protection of live stock against the disease through treatment mastitis post-milking TeatDipping. This productis more economical prices so that farmers do not spend a lotto take care of their animals. "BIO-MASTIC" has great potential to be developed areas such as dairy cattle centers in poor districts and Kota batu and can earn big profit. The Progress of programs divided into six stages including market research and planning, the purchase of means of production, the search for raw materials, implementing production, testing and marketing of products. Stage of market research conducted in the central areas of the dairy farm, the method used is to interview farmers to dairy farmers. Production Stage conducted in the Laboratory of FKM(Microtechnic Physiology and Plant Tissue Culture, the amount of production for 4 months obtained 248 liters. Stage product testing carried out in the laboratory of FKM (Physiology, Plant Tissue culture and Microtechnic) Faculty of Biology and Bacteriology laboratory Brawijaya University. at the marketing stage, we aim at a target market that is central areas of the dairy farm. Mean while applied marketing strategy is to go to the breeder directly and in cooperation with Prosperous UD.Sumber. Moreover, we follow the bazaars both campus and national levels. "BIO-MASTIC" business innovation antiseptict eat dipping first in Indonesia in the field of prospective and sustainable farms, so as to address the needs of animals in an effort to overcome the problems of lack of antiseptics for milking. hoped would also createa goodbrand image and product support antiseptic"BIO- MASTIC", so it has the potential to be commercialized in Indonesia. Keywords : Mastitis, Natural Protection, Teat Dipping, profitable, sustainable.

Research paper thumbnail of Wild type p53 function in p53 Y220C mutant harboring cells by treatment with Ashwagandha derived anticancer withanolides: bioinformatics and experimental evidence

Research paper thumbnail of Novel Ca↵eic Acid Phenethyl Ester-Mortalin Antibody Nanoparticles O↵er Enhanced Selective Cytotoxicity to Cancer Cells

Cancer, BAsel (MDPI), 2020

Ca↵eic acid phenethyl ester (CAPE) is a key bioactive ingredient of honeybee propolis and is clai... more Ca↵eic acid phenethyl ester (CAPE) is a key bioactive ingredient of honeybee propolis and is claimed to have anticancer activity. Since mortalin, a hsp70 chaperone, is enriched in a cancerous cell surface, we recruited a unique cell internalizing anti-mortalin antibody (MotAb) to generate mortalin-targeting CAPE nanoparticles (CAPE-MotAb). Biophysical and biomolecular analyses revealed enhanced anticancer activity of CAPE-MotAb both in in vitro and in vivo assays. We demonstrate that CAPE-MotAb cause a stronger dose-dependent growth arrest/apoptosis of cancer cells through the downregulation of Cyclin D1-CDK4, phospho-Rb, PARP-1, and anti-apoptotic protein Bcl2. Concomitantly, a significant increase in the expression of p53, p21 WAF1 , and caspase cleavage was obtained only in CAPE-MotAb treated cells. We also demonstrate that CAPE-MotAb caused a remarkably enhanced downregulation of proteins critically involved in cell migration. In vivo tumor growth assays for subcutaneous xenografts in nude mice also revealed a significantly enhanced suppression of tumor growth in the treated group suggesting that these novel CAPE-MotAb nanoparticles may serve as a potent anticancer nanomedicine.

Research paper thumbnail of Combination of Withaferin-A and CAPE Provides Superior Anticancer Potency: Bioinformatics and Experimental Evidence to Their Molecular Targets and Mechanism of Action

Cancers, Basel (MDPI), 2020

We have earlier reported anticancer activity in Withaferin A (Wi-A), a withanolide derived from A... more We have earlier reported anticancer activity in Withaferin A (Wi-A), a withanolide derived from Ashwagandha (Withania somnifera) and ca↵eic acid phenethyl ester (CAPE), an active compound from New Zealand honeybee propolis. Whereas Wi-A was cytotoxic to both cancer and normal cells, CAPE has been shown to cause selective death of cancer cells. In the present study, we investigated the e cacy of Wi-A, CAPE, and their combination to ovarian and cervical cancer cells. Both Wi-A and CAPE were seen to activate tumor suppressor protein p53 by downregulation of mortalin and abrogation of its interactions with p53. Downregulation of mortalin translated to compromised mitochondria integrity and function that a↵ected poly ADP-ribose polymerase1 (PARP1); a key regulator of DNA repair and protein-target for Olaparib, drugs clinically used for treatment of breast, ovarian and cervical cancers)-mediated DNA repair yielding growth arrest or apoptosis. Furthermore, we also compared the docking capability of Wi-A and CAPE to PARP1 and found that both of these could bind to the catalytic domain of PARP1, similar to Olaparib. We provide experimental evidences that (i) Wi-A and CAPE cause inactivation of PARP1-mediated DNA repair leading to accumulation of DNA damage and activation of apoptosis signaling by multiple ways, and (ii) a combination of Wi-A and CAPE o↵ers selective toxicity and better potency to cancer cells.

Research paper thumbnail of Combination of Withaferin-A and CAPE Provides Superior Anticancer Potency: Bioinformatics and Experimental Evidence to Their Molecular Targets and Mechanism of Action

CANCERS. Basel, 2020

We have earlier reported anticancer activity in Withaferin A (Wi-A), a withanolide derived from A... more We have earlier reported anticancer activity in Withaferin A (Wi-A), a withanolide derived from Ashwagandha (Withania somnifera) and ca↵eic acid phenethyl ester (CAPE), an active compound from New Zealand honeybee propolis. Whereas Wi-A was cytotoxic to both cancer and normal cells, CAPE has been shown to cause selective death of cancer cells. In the present study, we investigated the e cacy of Wi-A, CAPE, and their combination to ovarian and cervical cancer cells. Both Wi-A and CAPE were seen to activate tumor suppressor protein p53 by downregulation of mortalin and abrogation of its interactions with p53. Downregulation of mortalin translated to compromised mitochondria integrity and function that a↵ected poly ADP-ribose polymerase1 (PARP1); a key regulator of DNA repair and protein-target for Olaparib, drugs clinically used for treatment of breast, ovarian and cervical cancers)-mediated DNA repair yielding growth arrest or apoptosis. Furthermore, we also compared the docking capability of Wi-A and CAPE to PARP1 and found that both of these could bind to the catalytic domain of PARP1, similar to Olaparib. We provide experimental evidences that (i) Wi-A and CAPE cause inactivation of PARP1-mediated DNA repair leading to accumulation of DNA damage and activation of apoptosis signaling by multiple ways, and (ii) a combination of Wi-A and CAPE o↵ers selective toxicity and better potency to cancer cells.

Research paper thumbnail of Mutant p53L194F Harboring Luminal-A Breast Cancer Cells Are Refractory to Apoptosis and Cell Cycle Arrest in Response to MortaparibPlus, a Multimodal Small Molecule Inhibitor

Cancers, 2021

Simple Summary Tumor suppressor protein p53 is a master regulator that inhibits the process of on... more Simple Summary Tumor suppressor protein p53 is a master regulator that inhibits the process of oncogenesis by induction of cell senescence/cell cycle arrest/apoptosis during normal and stressed states of cells. It is functionally inactivated in the majority of cancers. Mortalin, a member of the Hsp70 family of proteins, enriched in cancer cells, is known to cause cytoplasmic sequestration and inactivation of the p53’s transcriptional activation function. Inhibition of mortalin–p53 interaction and reactivation of p53 functions by natural and synthetic drugs has emerged as a possible cancer therapeutic strategy. We recently reported a novel multimodal small molecule, named MortaparibPlus, that inhibited mortalin–p53 interaction and caused reactivation of p53 function in colorectal cancer cells. Here, we report its effect on breast cancer cells with wildtype (MCF-7) or mutant (T47D) p53 status. Abstract We previously performed a drug screening to identify a potential inhibitor of morta...

Research paper thumbnail of Antibody production of wild-type and enzyme V279F variants of PAF-AH as a risk factor for Cardiovascular disease

Coronary artery disease (CAD) has emerged as a leading cause of death in Indonesia nowadays. WHO ... more Coronary artery disease (CAD) has emerged as a leading cause of death in Indonesia nowadays. WHO data in 2012 revealed that 37% of the Indonesian population died from this disease. CAD occurs because of endothelial dysfunction in the arteries. Lipoprotein-associated phospholipase A2 (Lp-PLA2), also known as platelet-activating factor acetylhydrolase (PAF-AH), is a phospholipase A2 enzyme, encoded by the PLA2G7 gene. This protein is predicted to be involved in inflammatory phospholipid metabolism so it can be used as a biomarker of CAD in the early phase. Thus, the purpose of this research is to discover the difference in antibody production between wild-type and mutant V279F. The PAF-AH enzyme was isolated from mice lymphocyte cells in order to develop this enzyme as a biomarker of cardiovascular disease. PAF-AH migrates at 55kDa according to SDS-PAGE analysis. Flow cytometry analysis showed that mutant PAF-AH (V279F) is more antigenic than wild-type PAF-AH. The missense mutation of...

Research paper thumbnail of Functional characterization of miR-708 microRNA in telomerase positive and negative human cancer cells

Scientific Reports, 2021

Activation of a telomere length maintenance mechanism (TMM), including telomerase and alternative... more Activation of a telomere length maintenance mechanism (TMM), including telomerase and alternative lengthening of telomeres (ALT), is essential for replicative immortality of tumor cells, although its regulatory mechanisms are incompletely understood. We conducted a microRNA (miRNA) microarray analysis on isogenic telomerase positive (TEP) and ALT cancer cell lines. Amongst nine miRNAs that showed difference in their expression in TEP and ALT cancer cells in array analysis, miR-708 was selected for further analysis since it was consistently highly expressed in a large panel of ALT cells. miR-708 in TEP and ALT cancer cells was not correlated with C-circle levels, an established feature of ALT cells. Its overexpression induced suppression of cell migration, invasion, and angiogenesis in both TEP and ALT cells, although cell proliferation was inhibited only in TEP cells suggesting that ALT cells may have acquired the ability to escape inhibition of cell proliferation by sustained miR-7...

Research paper thumbnail of Computational and in vitro experimental analyses of the Anti-COVID-19 potential of Mortaparib and MortaparibPlus

Bioscience Reports

COVID-19 pandemic caused by SARS-CoV-2 virus has become a global health emergency. Although new v... more COVID-19 pandemic caused by SARS-CoV-2 virus has become a global health emergency. Although new vaccines have been generated and being implicated, discovery and application of novel preventive and control measures are warranted. We aimed to identify compound/s that may possess the potential to either block the entry of virus to host cells or attenuate its replication upon infection. Using host cell surface receptor expression (Angiotensin-converting enzyme 2 (ACE2) and Transmembrane protease serine 2 (TMPRSS2) analysis as an assay, we earlier screened several synthetic and natural compounds and identified candidates that showed ability to downregulate their expression. Here, we report experimental and computational analyses of two small molecules, Mortaparib and MortaparibPlus that were initially identified as dual novel inhibitors of mortalin and PARP-1, for their activity against SARS-CoV-2. In silico analyses showed that MortaparibPlus, but not Mortaparib, stably binds into the c...

Research paper thumbnail of Identification and Characterization of MortaparibPlus—A Novel Triazole Derivative That Targets Mortalin-p53 Interaction and Inhibits Cancer-Cell Proliferation by Wild-Type p53-Dependent and -Independent Mechanisms

Cancers

p53 has an essential role in suppressing the carcinogenesis process by inducing cell cycle arrest... more p53 has an essential role in suppressing the carcinogenesis process by inducing cell cycle arrest/apoptosis/senescence. Mortalin/GRP75 is a member of the Hsp70 protein family that binds to p53 causing its sequestration in the cell cytoplasm. Hence, p53 cannot translocate to the nucleus to execute its canonical tumour suppression function as a transcription factor. Abrogation of mortalin-p53 interaction and subsequent reactivation of p53’s tumour suppression function has been anticipated as a possible approach in developing a novel cancer therapeutic drug candidate. A chemical library was screened in a high-content screening system to identify potential mortalin-p53 interaction disruptors. By four rounds of visual assays for mortalin and p53, we identified a novel synthetic small-molecule triazole derivative (4-[(1E)-2-(2-phenylindol-3-yl)-1-azavinyl]-1,2,4-triazole, henceforth named MortaparibPlus). Its activities were validated using multiple bioinformatics and experimental approac...

Research paper thumbnail of BIO-MASTIC (Mastitis Natural Antiseptic), Pemanfaatan Ekstrak Daun Kersen sebagai Antiseptik Tear Dipping

"BIO-MASTIC" is based natural antiseptic compounds containing antibacterial protection ... more "BIO-MASTIC" is based natural antiseptic compounds containing antibacterial protection cherry leaves. thing more support in making this antiseptic is a special antiseptic product innovation Teat Dipping that has never existed in the market, another advantage with natural ingredients that have been tested, so as to provide protection of live stock against the disease through treatment mastitis post-milking TeatDipping. This productis more economical prices so that farmers do not spend a lotto take care of their animals. "BIO-MASTIC" has great potential to be developed areas such as dairy cattle centers in poor districts and Kota batu and can earn big profit. The Progress of programs divided into six stages including market research and planning, the purchase of means of production, the search for raw materials, implementing production, testing and marketing of products. Stage of market research conducted in the central areas of the dairy farm, the method used is to interview farmers to dairy farmers. Production Stage conducted in the Laboratory of FKM(Microtechnic Physiology and Plant Tissue Culture, the amount of production for 4 months obtained 248 liters. Stage product testing carried out in the laboratory of FKM (Physiology, Plant Tissue culture and Microtechnic) Faculty of Biology and Bacteriology laboratory Brawijaya University. at the marketing stage, we aim at a target market that is central areas of the dairy farm. Mean while applied marketing strategy is to go to the breeder directly and in cooperation with Prosperous UD.Sumber. Moreover, we follow the bazaars both campus and national levels. "BIO-MASTIC" business innovation antiseptict eat dipping first in Indonesia in the field of prospective and sustainable farms, so as to address the needs of animals in an effort to overcome the problems of lack of antiseptics for milking. hoped would also createa goodbrand image and product support antiseptic"BIO- MASTIC", so it has the potential to be commercialized in Indonesia. Keywords : Mastitis, Natural Protection, Teat Dipping, profitable, sustainable.

Research paper thumbnail of Wild type p53 function in p53 Y220C mutant harboring cells by treatment with Ashwagandha derived anticancer withanolides: bioinformatics and experimental evidence

Research paper thumbnail of Novel Ca↵eic Acid Phenethyl Ester-Mortalin Antibody Nanoparticles O↵er Enhanced Selective Cytotoxicity to Cancer Cells

Cancer, BAsel (MDPI), 2020

Ca↵eic acid phenethyl ester (CAPE) is a key bioactive ingredient of honeybee propolis and is clai... more Ca↵eic acid phenethyl ester (CAPE) is a key bioactive ingredient of honeybee propolis and is claimed to have anticancer activity. Since mortalin, a hsp70 chaperone, is enriched in a cancerous cell surface, we recruited a unique cell internalizing anti-mortalin antibody (MotAb) to generate mortalin-targeting CAPE nanoparticles (CAPE-MotAb). Biophysical and biomolecular analyses revealed enhanced anticancer activity of CAPE-MotAb both in in vitro and in vivo assays. We demonstrate that CAPE-MotAb cause a stronger dose-dependent growth arrest/apoptosis of cancer cells through the downregulation of Cyclin D1-CDK4, phospho-Rb, PARP-1, and anti-apoptotic protein Bcl2. Concomitantly, a significant increase in the expression of p53, p21 WAF1 , and caspase cleavage was obtained only in CAPE-MotAb treated cells. We also demonstrate that CAPE-MotAb caused a remarkably enhanced downregulation of proteins critically involved in cell migration. In vivo tumor growth assays for subcutaneous xenografts in nude mice also revealed a significantly enhanced suppression of tumor growth in the treated group suggesting that these novel CAPE-MotAb nanoparticles may serve as a potent anticancer nanomedicine.

Research paper thumbnail of Combination of Withaferin-A and CAPE Provides Superior Anticancer Potency: Bioinformatics and Experimental Evidence to Their Molecular Targets and Mechanism of Action

Cancers, Basel (MDPI), 2020

We have earlier reported anticancer activity in Withaferin A (Wi-A), a withanolide derived from A... more We have earlier reported anticancer activity in Withaferin A (Wi-A), a withanolide derived from Ashwagandha (Withania somnifera) and ca↵eic acid phenethyl ester (CAPE), an active compound from New Zealand honeybee propolis. Whereas Wi-A was cytotoxic to both cancer and normal cells, CAPE has been shown to cause selective death of cancer cells. In the present study, we investigated the e cacy of Wi-A, CAPE, and their combination to ovarian and cervical cancer cells. Both Wi-A and CAPE were seen to activate tumor suppressor protein p53 by downregulation of mortalin and abrogation of its interactions with p53. Downregulation of mortalin translated to compromised mitochondria integrity and function that a↵ected poly ADP-ribose polymerase1 (PARP1); a key regulator of DNA repair and protein-target for Olaparib, drugs clinically used for treatment of breast, ovarian and cervical cancers)-mediated DNA repair yielding growth arrest or apoptosis. Furthermore, we also compared the docking capability of Wi-A and CAPE to PARP1 and found that both of these could bind to the catalytic domain of PARP1, similar to Olaparib. We provide experimental evidences that (i) Wi-A and CAPE cause inactivation of PARP1-mediated DNA repair leading to accumulation of DNA damage and activation of apoptosis signaling by multiple ways, and (ii) a combination of Wi-A and CAPE o↵ers selective toxicity and better potency to cancer cells.

Research paper thumbnail of Combination of Withaferin-A and CAPE Provides Superior Anticancer Potency: Bioinformatics and Experimental Evidence to Their Molecular Targets and Mechanism of Action

CANCERS. Basel, 2020

We have earlier reported anticancer activity in Withaferin A (Wi-A), a withanolide derived from A... more We have earlier reported anticancer activity in Withaferin A (Wi-A), a withanolide derived from Ashwagandha (Withania somnifera) and ca↵eic acid phenethyl ester (CAPE), an active compound from New Zealand honeybee propolis. Whereas Wi-A was cytotoxic to both cancer and normal cells, CAPE has been shown to cause selective death of cancer cells. In the present study, we investigated the e cacy of Wi-A, CAPE, and their combination to ovarian and cervical cancer cells. Both Wi-A and CAPE were seen to activate tumor suppressor protein p53 by downregulation of mortalin and abrogation of its interactions with p53. Downregulation of mortalin translated to compromised mitochondria integrity and function that a↵ected poly ADP-ribose polymerase1 (PARP1); a key regulator of DNA repair and protein-target for Olaparib, drugs clinically used for treatment of breast, ovarian and cervical cancers)-mediated DNA repair yielding growth arrest or apoptosis. Furthermore, we also compared the docking capability of Wi-A and CAPE to PARP1 and found that both of these could bind to the catalytic domain of PARP1, similar to Olaparib. We provide experimental evidences that (i) Wi-A and CAPE cause inactivation of PARP1-mediated DNA repair leading to accumulation of DNA damage and activation of apoptosis signaling by multiple ways, and (ii) a combination of Wi-A and CAPE o↵ers selective toxicity and better potency to cancer cells.

Research paper thumbnail of Mutant p53L194F Harboring Luminal-A Breast Cancer Cells Are Refractory to Apoptosis and Cell Cycle Arrest in Response to MortaparibPlus, a Multimodal Small Molecule Inhibitor

Cancers, 2021

Simple Summary Tumor suppressor protein p53 is a master regulator that inhibits the process of on... more Simple Summary Tumor suppressor protein p53 is a master regulator that inhibits the process of oncogenesis by induction of cell senescence/cell cycle arrest/apoptosis during normal and stressed states of cells. It is functionally inactivated in the majority of cancers. Mortalin, a member of the Hsp70 family of proteins, enriched in cancer cells, is known to cause cytoplasmic sequestration and inactivation of the p53’s transcriptional activation function. Inhibition of mortalin–p53 interaction and reactivation of p53 functions by natural and synthetic drugs has emerged as a possible cancer therapeutic strategy. We recently reported a novel multimodal small molecule, named MortaparibPlus, that inhibited mortalin–p53 interaction and caused reactivation of p53 function in colorectal cancer cells. Here, we report its effect on breast cancer cells with wildtype (MCF-7) or mutant (T47D) p53 status. Abstract We previously performed a drug screening to identify a potential inhibitor of morta...

Research paper thumbnail of Antibody production of wild-type and enzyme V279F variants of PAF-AH as a risk factor for Cardiovascular disease

Coronary artery disease (CAD) has emerged as a leading cause of death in Indonesia nowadays. WHO ... more Coronary artery disease (CAD) has emerged as a leading cause of death in Indonesia nowadays. WHO data in 2012 revealed that 37% of the Indonesian population died from this disease. CAD occurs because of endothelial dysfunction in the arteries. Lipoprotein-associated phospholipase A2 (Lp-PLA2), also known as platelet-activating factor acetylhydrolase (PAF-AH), is a phospholipase A2 enzyme, encoded by the PLA2G7 gene. This protein is predicted to be involved in inflammatory phospholipid metabolism so it can be used as a biomarker of CAD in the early phase. Thus, the purpose of this research is to discover the difference in antibody production between wild-type and mutant V279F. The PAF-AH enzyme was isolated from mice lymphocyte cells in order to develop this enzyme as a biomarker of cardiovascular disease. PAF-AH migrates at 55kDa according to SDS-PAGE analysis. Flow cytometry analysis showed that mutant PAF-AH (V279F) is more antigenic than wild-type PAF-AH. The missense mutation of...

Research paper thumbnail of Functional characterization of miR-708 microRNA in telomerase positive and negative human cancer cells

Scientific Reports, 2021

Activation of a telomere length maintenance mechanism (TMM), including telomerase and alternative... more Activation of a telomere length maintenance mechanism (TMM), including telomerase and alternative lengthening of telomeres (ALT), is essential for replicative immortality of tumor cells, although its regulatory mechanisms are incompletely understood. We conducted a microRNA (miRNA) microarray analysis on isogenic telomerase positive (TEP) and ALT cancer cell lines. Amongst nine miRNAs that showed difference in their expression in TEP and ALT cancer cells in array analysis, miR-708 was selected for further analysis since it was consistently highly expressed in a large panel of ALT cells. miR-708 in TEP and ALT cancer cells was not correlated with C-circle levels, an established feature of ALT cells. Its overexpression induced suppression of cell migration, invasion, and angiogenesis in both TEP and ALT cells, although cell proliferation was inhibited only in TEP cells suggesting that ALT cells may have acquired the ability to escape inhibition of cell proliferation by sustained miR-7...

Research paper thumbnail of Computational and in vitro experimental analyses of the Anti-COVID-19 potential of Mortaparib and MortaparibPlus

Bioscience Reports

COVID-19 pandemic caused by SARS-CoV-2 virus has become a global health emergency. Although new v... more COVID-19 pandemic caused by SARS-CoV-2 virus has become a global health emergency. Although new vaccines have been generated and being implicated, discovery and application of novel preventive and control measures are warranted. We aimed to identify compound/s that may possess the potential to either block the entry of virus to host cells or attenuate its replication upon infection. Using host cell surface receptor expression (Angiotensin-converting enzyme 2 (ACE2) and Transmembrane protease serine 2 (TMPRSS2) analysis as an assay, we earlier screened several synthetic and natural compounds and identified candidates that showed ability to downregulate their expression. Here, we report experimental and computational analyses of two small molecules, Mortaparib and MortaparibPlus that were initially identified as dual novel inhibitors of mortalin and PARP-1, for their activity against SARS-CoV-2. In silico analyses showed that MortaparibPlus, but not Mortaparib, stably binds into the c...

Research paper thumbnail of Identification and Characterization of MortaparibPlus—A Novel Triazole Derivative That Targets Mortalin-p53 Interaction and Inhibits Cancer-Cell Proliferation by Wild-Type p53-Dependent and -Independent Mechanisms

Cancers

p53 has an essential role in suppressing the carcinogenesis process by inducing cell cycle arrest... more p53 has an essential role in suppressing the carcinogenesis process by inducing cell cycle arrest/apoptosis/senescence. Mortalin/GRP75 is a member of the Hsp70 protein family that binds to p53 causing its sequestration in the cell cytoplasm. Hence, p53 cannot translocate to the nucleus to execute its canonical tumour suppression function as a transcription factor. Abrogation of mortalin-p53 interaction and subsequent reactivation of p53’s tumour suppression function has been anticipated as a possible approach in developing a novel cancer therapeutic drug candidate. A chemical library was screened in a high-content screening system to identify potential mortalin-p53 interaction disruptors. By four rounds of visual assays for mortalin and p53, we identified a novel synthetic small-molecule triazole derivative (4-[(1E)-2-(2-phenylindol-3-yl)-1-azavinyl]-1,2,4-triazole, henceforth named MortaparibPlus). Its activities were validated using multiple bioinformatics and experimental approac...