Down-Regulating Receptor Interacting Protein Kinase 1 (RIP1) Promotes Oxaliplatin-Induced Tca8113 Cell Apoptosis

Shan, Baozhong; Ma, Feng; Wang, MingGuo; Xu, Xin

doi:10.12659/msm.894184

Cited by 5 publications

(5 citation statements)

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“…46 Downregulation of RIPK1 promotes oxaliplatin-induced Tca8113 cell apoptosis. 47 The current study provides evidence that after treatment with miR-590-3p mimic, the expression level of NF-κB was decreased, and OS and inflammatory response were alleviated. Consistently, miR-590-3p transfection downregulates the activity of NF-κB and promotes cardiac function in experimental autoimmune myocarditis.…”

Section: Discussionmentioning

confidence: 52%

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Retracted: Overexpression of microRNA‐590‐3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF‐κB signaling pathway by binding to RIPK1

Zhao

Jiang

Wang

et al. 2018

J of Cellular Biochemistry

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Ischemic heart disease is widely considered as a major health threat, which causes a high number of deaths every year worldwide. Much evidence has shown that oxidative stress (OS) is implicated in the pathogenesis of ischemiareperfusion injury (IRI). This study aims to evaluate the effect of miR-590-3p on the OS of IRI mice through the nuclear factor kappa-B (NF-κB) signaling pathway by targeting receptor-interacting protein kinase 1 (RIPK1). IRI mouse models were established for extracting myocardial tissues and isolating myocardial cells. The expression of inflammatory related-factors was detected by enzyme-linked immunosorbent assay, and superoxide dismutase (SOD) and malondialdehyde (MDA) in tissues were determined. Reverse transcription quantitative polymerase chain reaction and Western blot analysis were performed to assess the role of miR-590-3p in the expression of NF-κB-related factors and apoptosis-related factors. Besides, the regulatory effects of miR-590-3p on myocardial cell proliferation and apoptosis were also assessed. According to the obtained results, we found that IRI mice displayed higher expression of tumor necrosis factor-α, interleukin (IL)-6, and interferon-γ, lower expression of IL-10 in serum, a decreased SOD level, and an increased MDA level. In addition, RIPK1 was determined as a target gene of miR-590-3p. After transfection of overexpressed miR-590-3p or si-RIPK1, declined RIPK1, NF-κB, Toll-like receptor 4, caspase-3, FasL, p53, and c-myc levels, increased B-cell lymphoma-2 level, promoted cell proliferation, promoted cell cycle distribution and inhibited apoptosis of myocardial cells were found. Our study demonstrates that miR-590-3p can alleviate the OS of IRI mice through the inhibition of the RIPK1 and NF-κB signaling pathway. Thus, miR-590-3p represents a potential target for IRI repair. K E Y W O R D S microRNA-590-3p, myocardial ischemia/reperfusion injury, nuclear factor kappa-B (NF-κB), oxidative stress (OS), receptor-interacting protein kinase 1 (RIPK1) J Cell Biochem. 2019;120:3559-3573.wileyonlinelibrary.com/journal/jcb Overexpression of microRNA-590-3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF-κB signaling pathway by binding to RIPK1.

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Section: Discussionmentioning

confidence: 52%

“…It is found that RIPK1 works as a potent promoter of cell apoptosis, and RIPK1 can also regulate NF‐κB and is likely necessary for NF‐κB activation . Downregulation of RIPK1 promotes oxaliplatin‐induced Tca8113 cell apoptosis …”

Section: Discussionmentioning

confidence: 99%

Retracted: Overexpression of microRNA‐590‐3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF‐κB signaling pathway by binding to RIPK1

Zhao

Jiang

Wang

et al. 2018

J of Cellular Biochemistry

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“…In recent years, it's also actively researched in castration resistant prostate cancer patients (29,30). Our data indicated that even cancer cells are resistant to ADT, they can be sensitive to chemotherapy, such as oxaliplatin due to its non-targeted cell death induction roles (31). In our syngeneic animal model of prostate cancer, either oxaliplatin or anti-PD-1 Ab increased overall survival marginally.…”

Section: Discussionmentioning

confidence: 68%

Chemotherapy oxaliplatin sensitizes prostate cancer to immune checkpoint blockade therapies via stimulating tumor immunogenicity

Zhou

Yang

Liu

et al. 2017

Molecular Medicine Reports

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Even though standard treatment options are available for prostate cancer patients, prostate cancer is still a leading cause of death in many Western countries due to drug resistance and recurrence. Immune checkpoint blockade therapy has been proved to be very effective in some melanoma patients, which might dependent on the preconditioned immune system. Here we explored the effect of chemotherapy (oxaliplatin) in combination with immune checkpoint blockade therapy (anti‑PD‑1 treatment) in prostate cancer cell lines and pre‑clinical animal models. We found that oxaliplatin is effective in castration‑resistant cells and enhanced the response of prostate cancer to anti‑PD‑1 antibody treatment. Oxaliplatin stimulated the immunogenic potential and established a pro‑immune microenvironment in prostate cancer. In conclusion, oxaliplatin sensitized anti‑PD‑1 treatment in prostate cancer and this combination may be an option for castration‑resistant prostate cancer patients.

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“…The present study is mainly limited by the lack of a comprehensive analysis of multiple proteins that could be involved in the effects of PARD3 expression on carcinogenesis of ESCC, such as connective tissue growth factor [ 30 ], interacting protein kinase 1 [ 31 ], cofilin-1, and transgelin [ 32 ]. In addition, only the PARD3 protein was studied, and there could be some discrepancies between transcription and translation.…”

Section: Discussionmentioning

confidence: 99%

Partition-Defective 3 (PARD3) Regulates Proliferation, Apoptosis, Migration, and Invasion in Esophageal Squamous Cell Carcinoma Cells

et al. 2017

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BackgroundAltered expression of partition-defective 3 (PARD3), a polarity-related gene associated with oncogenesis, has been identified in some cancers, but the role of PARD3 in esophageal squamous cell carcinoma (ESCC) remains unclear.Material/MethodsPARD3 expression in Eca109 cells was silenced using siRNA and overexpressed using an expression vector. We investigated the role of PARD3 in ESCC growth and motility to evaluate its potential role in ESCC. Transwell assay was used to evaluated cell migration and invasion. PARD3 protein expression was assessed by Western blot.ResultsPARD3 overexpression promoted apoptosis, impaired proliferation, and inhibited cell migration and invasion in Eca109 cells, while PARD3 silencing promoted proliferation and increased migration and invasion. Overexpression of PARD3 exerted its antitumor activity in vitro by impairing cell proliferation, inducing apoptosis, and inhibiting migration and invasion of Eca109 cells, suggesting that PARD3 might play a tumor suppressor role in ESCC.ConclusionsOverexpression of PARD3 could be a promising new therapeutic intervention against ESCC.

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Down-Regulating Receptor Interacting Protein Kinase 1 (RIP1) Promotes Oxaliplatin-Induced Tca8113 Cell Apoptosis

Cited by 5 publications

References 20 publications

Retracted: Overexpression of microRNA‐590‐3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF‐κB signaling pathway by binding to RIPK1

Retracted: Overexpression of microRNA‐590‐3p promotes the proliferation of and inhibits the apoptosis of myocardial cells through inhibition of the NF‐κB signaling pathway by binding to RIPK1

Chemotherapy oxaliplatin sensitizes prostate cancer to immune checkpoint blockade therapies via stimulating tumor immunogenicity

Partition-Defective 3 (PARD3) Regulates Proliferation, Apoptosis, Migration, and Invasion in Esophageal Squamous Cell Carcinoma Cells

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