Mitochondrial division inhibitor-1 potentiates cisplatin-induced apoptosis via the mitochondrial death pathway in cholangiocarcinoma cells

Tusskorn, Ornanong; Khunluck, Tueanjai; Prawan, Auemduan; Senggunprai, Laddawan; Kukongviriyapan, Veerapol

doi:10.1016/j.biopha.2018.12.051

Cited by 46 publications

(33 citation statements)

References 35 publications

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“…Salinomycin (a naturally occurring polyether antibiotic [138]), capsaicin (a major pungent component of chili pepper [139]), oblongifolin C (a natural small molecule extracted from Garcinia yunnanensis Hu [140]) and resveratrol (a natural phenol, phytoalexin, produced by plants against infections [30]) have shown anticancer efficacy on CCA models by different mechanisms: inhibiting autophagosome fusion to lysosomes, promoting mTOR activation and blocking ATG7 activation, respectively. Two class III PI3K inhibitors that block initiation of autophagy (3-MA and wortmannin [106]) and Mdivi1 (selective Drp-1 inhibitor [141]), which interferes with mitochondrial activity, have also shown efficacy on CCA.…”

Section: Autophagy Inhibitorsmentioning

confidence: 99%

“…GNS561 promotes lysosomal dysregulation through lysosome permeabilization and release of hydrolytic enzymes to the cytosol, leading to the impairment of autophagosome fusion to lysosome and induction of apoptosis in vivo in iCCA xenografts [137]. Mdivi-1 is thought to act inhibiting enlongation of autophagosomes impeding mitochondrial dynamics, leading to autophagy inhibition that potentiates cisplatin-induced apoptosis in CCA [141].…”

Section: Autophagy Inhibitorsmentioning

confidence: 99%

“…A wide variety of anticancer compounds induce autophagy in CCA, making it necessary to discern whether it is a protective autophagy promoted by cancer cells as an adaptive mechanism, therefore inhibition of autophagy leads to a potentiation of their cytotoxic effects, or if on the contrary, mediates drug mechanism of cancer cell death induction. Several compounds that show anticancer efficacy on CCA cells such as norcantharidin [145], compound C [146], vorinostat [147] or cisplatin [106,141] induce the activation of protective autophagy in CCA cells, and pharmacological inhibition of autophagic process enhances these drugs anti-cancer capacity, accelerating apoptosis and sensitizing cell to chemotherapy. The combination of these drugs with autophagy inhibitors offers an attractive therapeutic strategy.…”

Section: Autophagy Inhibitorsmentioning

confidence: 99%

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Therapeutic Potential of Autophagy Modulation in Cholangiocarcinoma

Pérez‐Montoyo

2020

Cells

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Autophagy is a multistep catabolic process through which misfolded, aggregated or mutated proteins and damaged organelles are internalized in membrane vesicles called autophagosomes and ultimately fused to lysosomes for degradation of sequestered components. The multistep nature of the process offers multiple regulation points prone to be deregulated and cause different human diseases but also offers multiple targetable points for designing therapeutic strategies. Cancer cells have evolved to use autophagy as an adaptive mechanism to survive under extremely stressful conditions within the tumor microenvironment, but also to increase invasiveness and resistance to anticancer drugs such as chemotherapy. This review collects clinical evidence of autophagy deregulation during cholangiocarcinogenesis together with preclinical reports evaluating compounds that modulate autophagy to induce cholangiocarcinoma (CCA) cell death. Altogether, experimental data suggest an impairment of autophagy during initial steps of CCA development and increased expression of autophagy markers on established tumors and in invasive phenotypes. Preclinical efficacy of autophagy modulators promoting CCA cell death, reducing invasiveness capacity and resensitizing CCA cells to chemotherapy open novel therapeutic avenues to design more specific and efficient strategies to treat this aggressive cancer.

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Section: Autophagy Inhibitorsmentioning

confidence: 99%

Section: Autophagy Inhibitorsmentioning

confidence: 99%

Section: Autophagy Inhibitorsmentioning

confidence: 99%

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Therapeutic Potential of Autophagy Modulation in Cholangiocarcinoma

Pérez‐Montoyo

2020

Cells

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“…Cisplatin induces high ROS levels that cause cancer cell apoptosis [14]. In addition, ROS can indirectly regulate CDDP-induced apoptosis and autophagy and exhibit potential chemosensitization in various malignancies including cholangiocarcinoma [15], lung cancer [16], and malignant mesothelioma [17]. Mechanism studies have revealed that plumbagin induces cytotoxicity in various cancers, such as cervical cancer [18] and breast cancer [19], by producing ROS.…”

Section: Introductionmentioning

confidence: 99%

Plumbagin Enhances the Anticancer Efficacy of Cisplatin by Increasing Intracellular ROS in Human Tongue Squamous Cell Carcinoma

Xue

Pan

Zhou

et al. 2020

Oxidative Medicine and Cellular Longevity

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Cisplatin is widely used in the treatment of tongue squamous cell carcinoma (TSCC), but its clinical efficacy is limited by drug resistance and toxic side effects. Hence, a novel compound capable of enhancing the anticancer effect of cisplatin while reducing the side effects is urgently needed. We have previously shown that plumbagin (PLB), an anticancer phytochemical, is able to inhibit the growth of TSCC in vitro and in vivo. The objective of this study was to investigate the effect of PLB in reversing the resistance of TSCC to cisplatin as well as its molecular mechanisms. Here, we found that PLB enhances cisplatin-induced cytotoxicity, apoptosis, and autophagy in CAL27 and cisplatin-resistant CAL27/CDDP cells. PLB could inhibit the viability and growth of TSCC cells by increasing the production of intracellular reactive oxygen species (ROS). In addition, the combination treatment of PLB and cisplatin resulted in a synergistic inhibition of TSCC viability, apoptosis, and autophagy by increasing intracellular ROS, which may be achieved by activating JNK and inhibiting AKT/mTOR signaling pathways. Finally, the synergistic treatment was also demonstrated in vivo. Therefore, PLB combined with cisplatin is a potential therapeutic strategy against therapy TSCC cisplatin resistance.

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“…As cisplatin damages cellular DNA, cisplatin induces mitochondrial apoptosis of cancer cells. 36,37 TAZ is involved in maintaining the stability of mitochondrial outer membrane to keep the MMP. 38 Thus, reduction of TAZ expression can decrease the stability of mitochondrial outer membrane to facilitate the mitochondrial pathway of apoptosis.…”

Section: Discussionmentioning

confidence: 99%

<p>Restoration of miR-26b expression partially reverses the cisplatin resistance of NSCLC by targeting tafazzin</p>

Zang

Zhao

Gao

et al. 2019

OTT

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Background: Dysregulation of microRNAs has been reported to be responsible for drug resistance of cancers. However, the association between aberrant expression of miR-26b and cisplatin resistance in non-small cell lung cancer (NSCLC) remains unclear. Methods: PC9 and A549 were used to establish the cisplatin resistance models on NSCLC. Expression of miR-26b in cisplatin-resistant PC9 and A549 cells (PC9/R and A549/R) was detected by quantitative real-time PCR assays. Drug sensitivity and mitochondrial apoptosis were detected by Cell Counting Kit-8 assay and flow cytometry assay, respectively. The target relationship between miR-26b and tafazzin (TAZ) was validated by dual-luciferase reporter assay. Results: Obvious downregulation of miR-26b was observed in PC9/R and A549/R cells. Restoration of miR-26b partially reversed the cisplatin resistance of PC9/R and A549/R cells. Expression of TAZ was increased in PC9/R and A549/R cells compared to the parental PC9 and A549 cells. Results of dual-luciferase reporter assays verified that TAZ was targeted by miR-26b. We showed that restoration of miR-26b expression inhibited the TAZ expression and thus expanded the mitochondrial pathway of apoptosis induced by cisplatin in PC9/ R and A549/R cells. Conclusion: Restoration of miR-26b expression partially reverses the cisplatin resistance of NSCLC by targeting TAZ. miR-26b/TAZ axis may represent a potential strategy to reverse the cisplatin in NSCLC.

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Mitochondrial division inhibitor-1 potentiates cisplatin-induced apoptosis via the mitochondrial death pathway in cholangiocarcinoma cells

Cited by 46 publications

References 35 publications

Therapeutic Potential of Autophagy Modulation in Cholangiocarcinoma

Therapeutic Potential of Autophagy Modulation in Cholangiocarcinoma

Plumbagin Enhances the Anticancer Efficacy of Cisplatin by Increasing Intracellular ROS in Human Tongue Squamous Cell Carcinoma

<p>Restoration of miR-26b expression partially reverses the cisplatin resistance of NSCLC by targeting tafazzin</p>

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