Opa-interacting protein 5 modulates docetaxel-induced cell death via regulation of mitophagy in gastric cancer

Kim, Tae Woo; Lee, Seon-Jin; Park, Young-Jun; Park, Soo‐Jin; Oh, Byung Moo; Park, Yun Sun; Kim, Bo-Yeon; Lee, Young-Ha; Cho, Hee Jun; Yoon, Suk Ran; Choe, Yong-Kyung; Lee, Hee Gu

doi:10.1177/1010428317733985

Cited by 15 publications

(8 citation statements)

References 56 publications

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“…He et al found that suppression of OIP5 increased the cell population of the G1 phase in 5637 cell lines of BC 13. Additionally, OIP5 repressed docetaxel-induced mitochondrial damage by modulating the mitophagy pathway49. These studies robustly suggested that OIP5 play an important role in cells mitosis, involved in DNA replication, chromosome maintenance.…”

Section: Discussionmentioning

confidence: 94%

OIP5 Promotes Growth, Metastasis and Chemoresistance to Cisplatin in Bladder Cancer Cells

Wang¹,

Chen²,

Fan³

et al. 2018

J. Cancer

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Opa interacting protein 5 (OIP5) has previously been identified as a tumorigenesis gene. The purpose of this study is to explore the role of OIP5 in the progression of bladder cancer (BC). The OIP5 expression and clinical behaviors in bladder cancer were collected from lager database. Our study showed that OIP5 was highly expressed in bladder cancer tissues and cells. Overexpression of OIP5 in tumor patients predicted worse overall survival (OS) and higher histological grade. Vitro and vivo experiments demonstrated that knockdown of OIP5 significantly inhibited cell growth of BC. Scratch assay and transwell assay suggested that migration capacity of BC cells was decreased after knockdown of OIP5. Cisplatin sensitivity assay indicated that depletion of OIP5 increased the sensitivity of BC cells to cisplatin. Finally, we identified 38 overlapping differentially expressed genes (DEGs) between RNA-seq and TCGA analyses which were closely linked to OIP5. Bioinformatics analysis showed that these DEGs enriched in oocyte meiosis, fanconi anemia pathway, cell cycle, and microRNAs regulation. TOP2A, SPAG5, SKA1, EXO1, TK1 were confirmed to associated with bladder cancer development. Our study suggests that OIP5 may be a potential biomarker for growth, metastasis and drug-resistance in bladder cancer.

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Section: Discussionmentioning

confidence: 94%

OIP5 Promotes Growth, Metastasis and Chemoresistance to Cisplatin in Bladder Cancer Cells

Wang¹,

Chen²,

Fan³

et al. 2018

J. Cancer

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“…Furthermore, OIP5 knockdown promoted the apoptosis of those cells. It was considered that cell apoptosis as an important physiological process is associated with the formation of a variety of tumor types (34,37). Thus, the aforementioned results indicated that OIP5 had important roles in the formation of liver cancer.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Opa interacting protein�5 increases the progression of liver cancer via BMPR2/JUN/CHEK1/RAC1 dysregulation

Xiao

et al. 2019

Oncol Rep

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Opa interacting protein 5 (OIP5) overexpression is associated with human carcinoma. However, its biological function, underlying mechanism and clinical significance in liver cancer remain unknown. In the present study, the effects of OIP5 expression on liver cancer, and the mechanisms regulating these effects, were investigated. OIP5 expression was measured in human hepatocellular carcinoma (HCC) tissues and liver cancer cell lines. The effect of OIP5 knockdown on tumorigenesis was also detected in nude mice, and differentially-expressed genes (DEGs) were identified and their biological functions were identified. The results indicated that OIP5 expression was significantly upregulated in HCC tissues and four liver cancer cell lines (P<0.01). Increased OIP5 protein expression significantly predicted reduced survival rate of patients with HCC (P<0.01). OIP5 knockdown resulted in the suppression of proliferation and colony forming abilities, cell cycle arrest at the G0/G1 or G2/M phases, and promotion of cell apoptosis. A total of 628 DEGs, including 87 upregulated and 541 downregulated genes, were identified following OIP5 knockdown. Functional enrichment analysis indicated that DEGs were involved in ‘RNA Post-Transcriptional Modification, Cancer and Organismal Injury and Abnormalities’. Finally, OIP5 knockdown in Huh7 cells dysregulated bone morphogenetic protein receptor type 2/JUN/checkpoint kinase 1/Rac family small GTPase 1 expression. In conclusion, the overall results demonstrated the involvement of OIP5 in the progression of liver cancer and its mechanism of action.

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“…For example, in docetaxel-treated prostate cancer cells, trehalose induces ULK1-independent mitophagy and reduces their sensitivity to their treatment [304]. Moreover, Opa-interacting protein 5 (OIP5) overexpression prevented docetaxel-induced cell death in gastric cancer cells by activating MFN2/PINK1-mediated mitophagy [305]. Instead, NIX-mediated mitophagy drives doxorubicin-resistance [306], whereas in the case of cisplatin/etoposide, the E3 ubiquitin-ligase ARIH1 -rather than Parkin- mediates PINK1-induced mitophagy of damaged mitochondria in response to cisplatin/etoposide [301].…”

Section: Mitophagy and Anti-cancer Therapiesmentioning

confidence: 99%

Mitophagy in Cancer: A Tale of Adaptation

Vara-Pérez

Felipe‐Abrio

Agostinis

2019

Cells

167

134

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In the past years, we have learnt that tumors co-evolve with their microenvironment, and that the active interaction between cancer cells and stromal cells plays a pivotal role in cancer initiation, progression and treatment response. Among the players involved, the pathways regulating mitochondrial functions have been shown to be crucial for both cancer and stromal cells. This is perhaps not surprising, considering that mitochondria in both cancerous and non-cancerous cells are decisive for vital metabolic and bioenergetic functions and to elicit cell death. The central part played by mitochondria also implies the existence of stringent mitochondrial quality control mechanisms, where a specialized autophagy pathway (mitophagy) ensures the selective removal of damaged or dysfunctional mitochondria. Although the molecular underpinnings of mitophagy regulation in mammalian cells remain incomplete, it is becoming clear that mitophagy pathways are intricately linked to the metabolic rewiring of cancer cells to support the high bioenergetic demand of the tumor. In this review, after a brief introduction of the main mitophagy regulators operating in mammalian cells, we discuss emerging cell autonomous roles of mitochondria quality control in cancer onset and progression. We also discuss the relevance of mitophagy in the cellular crosstalk with the tumor microenvironment and in anti-cancer therapy responses.

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Opa-interacting protein 5 modulates docetaxel-induced cell death via regulation of mitophagy in gastric cancer

Cited by 15 publications

References 56 publications

OIP5 Promotes Growth, Metastasis and Chemoresistance to Cisplatin in Bladder Cancer Cells

OIP5 Promotes Growth, Metastasis and Chemoresistance to Cisplatin in Bladder Cancer Cells

Overexpression of Opa interacting protein�5 increases the progression of liver cancer via BMPR2/JUN/CHEK1/RAC1 dysregulation

Mitophagy in Cancer: A Tale of Adaptation

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