Cisplatin based therapy: the role of the mitogen activated protein kinase signaling pathway

Achkar, Iman W; Abdulrahman, Nabeel; Al-Sulaiti, Hend; Joseph, Jensa Mariam; Uddin, Shahab; Mraiche, Fatima

doi:10.1186/s12967-018-1471-1

Cited by 161 publications

(100 citation statements)

References 103 publications

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“…It has been reported that cisplatin resistance in HCC may occur through the loss of Runt-associated transcription factor 3 and upregulation of cyclophilin B (21,22). Recently, certain key biomarkers of cisplatin resistance have revealed novel molecular mechanisms of resistance (23). The role of circRNAs in the development of chemotherapeutic drug resistance has also been highlighted (24-26).…”

Section: Discussionmentioning

confidence: 99%

Cisplatin resistance‑associated circRNA_101237 serves as a prognostic biomarker in hepatocellular carcinoma

et al. 2020

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Hepatocellular carcinoma (HCC) is a leading cause of cancer-associated mortality worldwide. Despite clinical advances, the survival rate of patients with HCC remains low, as most patients are diagnosed with HCC when they are already at the advanced stage. Certain circular RNAs (circRNAs) are closely associated with the development of liver cancer. In the present study, a circRNA array was performed to screen differentially expressed circRNAs in HCC tissues. The further analysis focused on the newly identified circRNA_101237, the host gene of which, cyclin-dependent kinase 8, is located at chr13:26974589-26975761. CircRNA_101237 was determined to be upregulated in tumor tissue and serum of patients with HCC as compared with that in paracancerous tissues and the serum of healthy controls, respectively. In addition, the expression of circRNA_101237 was associated with tumor size, lymph node metastasis, distant metastasis and TNM stage. Univariate and multivariate analysis indicated that serum circRNA_101237 levels were an independent predictor of survival prognosis in patients with HCC. The overall survival of patients with high expression of circRNA_101237 was reduced compared with that of patients with low expression of circRNA_101237. Of note, cisplatin induced the expression of circRNA_101237 in HCC cells in a dose-and time-dependent manner in vitro, and the levels of circRNA_101237 in the serum of patients with cisplatin-resistant HCC and in cisplatin-resistant Huh7 cells were increased. The present study provided novel insight into the use of circRNA_101237 as a diagnostic biomarker for HCC and a potential therapeutic target.

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Section: Discussionmentioning

confidence: 99%

Cisplatin resistance‑associated circRNA_101237 serves as a prognostic biomarker in hepatocellular carcinoma

et al. 2020

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“…Cisplatin (CP) is a potent antineoplastic agent that is widely used to treat various types of tumors (1,2). However, its clinical application is limited by time-and dose-dependent nephrotoxicity, which is associated with high morbidity and mortality (3,4).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of Histone H3K27 Acetylation Orchestrates Interleukin-9-Mediated and Plays an Anti-Inflammatory Role in Cisplatin-Induced Acute Kidney Injury

et al. 2020

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Nephrotoxicity is a major side effect of cisplatin (CP)-and platinum-related chemotherapy, and inflammation contributes to disease pathogenesis. Interleukin-9 (IL-9) is a pleiotropic cytokine associated with inflammation. Here, we investigated the key role of IL-9 as a regulator of protective mechanisms in CP-induced acute kidney injury (AKI). We observed that IL-9 was decreased not only in a CP-induced AKI mouse model but also in THP-1 and RAW264.7 cell lines. Seventy-two hours post-CP injection, renal dysfunction and tubule injury were significantly attenuated in IL-9 overexpression adeno-associated virus 9 (AAV9)-treated mice. The levels of serum urea, serum creatinine, kidney injury molecule-1 (KIM-1), and histological damage were partially diminished following treatment with IL-9. The renoprotective effects of IL-9 may be attributed to the regulation of cytokines, and we found that IL-9 acted on macrophages in a regulatory manner, promoting an anti-inflammatory phenotype. Furthermore, IL-9 enhanced the suppression of macrophage-driven renal inflammation. Inhibition of H3K27 acetylation orchestrated IL-9-mediated renoprotection in CP-induced AKI. Thus, our findings indicate novel and potent anti-inflammatory properties of IL-9 that confer preservation of kidney function and structure in CP-induced AKI, which may counteract kidney disease procession.

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“…2 The mammalian target of rapamycin (mTOR) is a serine/threonine protein kinase that controls cell proliferation and survival. Cisplatin triggers cell apoptosis by binding to DNA and crosslinking the DNA strands.…”

Section: Introductionmentioning

confidence: 99%

“…Several strategies can overcome cisplatin drug resistance and toxicity, including liposome delivery, inhibition of glutathione and metallothionein species, and combination therapy. 2 The mammalian target of rapamycin (mTOR) is a serine/threonine protein kinase that controls cell proliferation and survival. AKT1 overexpression and gene amplification have been shown to induce lung cancer cells to become resistant to cisplatin through mTOR signaling pathway.…”

Section: Introductionmentioning

confidence: 99%

Platinum‐based combination chemotherapy triggers cancer cell death through induction of BNIP3 and ROS, but not autophagy

Chung

Tang

et al. 2019

J Cellular Molecular Medi

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These days, cancer can still not be effectively cured because cancer cells readily develop resistance to anticancer drugs. Therefore, an effective combination of drugs with different mechanisms to prevent drug resistance has become a very important issue. Furthermore, the BH3-only protein BNIP3 is involved in both apoptotic and autophagic cell death. In this study, lung cancer cells were treated with a chemotherapy drug alone or in combination to identify the role of BNIP3 and autophagy in combination chemotherapy for treating cancer. Our data revealed that various combinational treatments of two drugs could increase cancer cell death and cisplatin in combination with rapamycin or LBH589, which triggered the cell cycle arrest at the S phase. Cells with autophagosome and pEGFP-LC3 puncta increased when treated with drugs. To confirm the role of autophagy, cancer cells were pre-treated with the autophagy inhibitor 3-methyladenine (3-MA). 3-MA sensitized cancer cells to chemotherapy drug treatments. These results suggest that autophagy may be responsible for cell survival in combination chemotherapy for lung cancer. Moreover, BNIP3 was induced and localized in mitochondria when cells were treated with drugs. The transfection of a dominant negative transmembrane deletion construct of BNIP3 (BNIP3ΔTM) and treatment of a reactive oxygen species (ROS) inhibitor suppressed chemo drug-induced cell death. These results indicate that BNIP3 and ROS may be involved in combination chemo drug-induced cell death. However, chemo drug-induced autophagy may protect cancer cells from drug cytotoxicity. As a result, inhibiting autophagy may improve the effects of combination chemotherapy when treating lung cancer. K E Y W O R D S autophagy, BNIP3, combination chemotherapy, reactive oxygen species How to cite this article: Chung L-Y, Tang S-J, Wu Y-C, et al. Platinum-based combination chemotherapy triggers cancer cell death through induction of Bnip3 and ROS, but not autophagy.

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Cisplatin based therapy: the role of the mitogen activated protein kinase signaling pathway

Cited by 161 publications

References 103 publications

Cisplatin resistance‑associated circRNA_101237 serves as a prognostic biomarker in hepatocellular carcinoma

Cisplatin resistance‑associated circRNA_101237 serves as a prognostic biomarker in hepatocellular carcinoma

Inhibition of Histone H3K27 Acetylation Orchestrates Interleukin-9-Mediated and Plays an Anti-Inflammatory Role in Cisplatin-Induced Acute Kidney Injury

Platinum‐based combination chemotherapy triggers cancer cell death through induction of BNIP3 and ROS, but not autophagy

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