CtIP promotes G2/M arrest in etoposide‐treated HCT116 cells in a p53‐independent manner

Chen, Hongyu; Shan, Jin; Chen, Dandan; Wang, Ruoxi; Qi, Wenjing; Wang, Hailong; Ke, Yueshuang; Liu, Wenguang; Zeng, Xianlu

doi:10.1002/jcp.27824

Cited by 7 publications

(7 citation statements)

References 44 publications

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“…23 Chen et al found that CtIP could promote G2/M phase arrest and enhance the cell sensitivity to Eto through the ATR/ Chk1/CDC25C pathway. 24 Our result also found that MRPL13 significantly decreased the component of M1 macrophages, CD8+ T cells, and CD4+ T cells in the NSCLC tumor microenvironment. Yuan et al suggested that M1 macrophages could suppress tumor development by inducing apoptosis, whereas M2a/M2c macrophages can promote lung cancer invasion and xenograft tumor growth.…”

supporting

confidence: 76%

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MRPL13 Act as a Novel Therapeutic Target and Could Promote Cell Proliferation in Non-Small Cell Lung Cancer

Jing¹,

Fu²,

Wang³

et al. 2021

CMAR

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Background:The latent involvement of MRPL13 in non-small cell lung cancer (NSCLC) remains unclear. This study aimed to explore the role of MRPL13 in NSCLC. Methods: All analyses were performed in R software 4.0, SPSS version 23, and GraphPad Prism 8. The "limma" package was used to identify differentially expressed genes. Univariate and multivariate cox analyses were used to identify prognosis-related genes. A549 and H1299 lung cancer cell lines were selected for phenotypic experiments.Results: The high level of MRPL13 was correlated with poor T classification and overall survival. In vitro experiments showed that MRPL13 was highly expressed in NSCLC tissue and cell lines. MRPL13 knockdown inhibited the proliferation of lung cancer A549 and H1299 cell lines, which was further validated by in vivo experiment. Moreover, GSEA analysis suggested that the pathway of MYC target, PI3K/AKT/mTOR/ signaling, oxidative phosphorylation, and G2/M checkpoints may be the potential pathway where MRPL13 was involved. Meanwhile, MRPL13 demonstrated a negative correlation with M1 macrophage, CD8+ T cells, and CD4+ T cells, making it an underlying immunotherapy target of NSCLC. Conclusion: MRPL13 may promote the proliferation of NSCLC cells and serve as an independent tumor marker and an emerging therapeutic target.

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supporting

confidence: 76%

“… 23 Chen et al found that CtIP could promote G2/M phase arrest and enhance the cell sensitivity to Eto through the ATR/Chk1/CDC25C pathway. 24 …”

Section: Discussionmentioning

confidence: 99%

MRPL13 Act as a Novel Therapeutic Target and Could Promote Cell Proliferation in Non-Small Cell Lung Cancer

Jing¹,

Fu²,

Wang³

et al. 2021

CMAR

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“…Subsequently, GLYR1 and MLH1 expression was calculated by multiplication of the percentage positivity score and staining intensity score, resulting in a final score ranging from 0 to 15. Accordingly, the final expression level of GLYR1 and MLH1 was defined as low (0-4), moderate (5)(6)(7)(8)(9) and high (10)(11)(12)(13)(14)(15). Ki-67 was positively located in the nucleus and appeared as brownish-yellow staining.…”

Section: Immunohistochemistry (Ihc) Analysismentioning

confidence: 99%

“…Studies on the regulatory mechanisms of p21 are focused mainly on p53dependent or p53-independent pathways. Most of these studies have indicated that p21 is directly targeted by p53, although more recent studies have indicated that p21 regulates cell cycle arrest, cell proliferation, apoptosis and other functions via a p53-independent pathway [12][13][14][15]. Furthermore, the well-characterized p38 mitogen-activated protein kinase (p38MAPK) and phosphatidyl 3-kinase/protein kinase B (PI3K/Akt) signaling pathways have been shown to be involved in the regulation of p21 [16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Downregulation of GLYR1 contributes to microsatellite instability colorectal cancer by targeting p21 via the p38MAPK and PI3K/AKT pathways

Long

et al. 2020

J Exp Clin Cancer Res

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Background: GLYR1 has a high mutation frequency in microsatellite instability colorectal cancer (MSI CRC) and is presumed to be a novel tumor suppressor. However, the role of GLYR1 in tumors has never been studied. In particular, the downregulation of GLYR1 in MSI CRC is worthy of further investigation. Methods: Western blot and immunohistochemistry analyses were used to detect GLYR1 protein expression in CRC tissues and cell lines, and the clinical significance of GLYR1 was also analyzed. The relationship between GLYR1 and MLH1 was validated by immunofluorescence, immunoprecipitation and bioinformatics analyses. Western blotting, qRT-PCR, CCK-8 assays, colony formation assays, flow cytometry and Hoechst 33258 staining assays were used to assess the effect of GLYR1 on the cell cycle progression, proliferation, differentiation and apoptosis of CRC cells in vitro. The related mechanisms were initially investigated by Western blotting. Results: GLYR1 was significantly downregulated in MSI CRC and its expression was negatively correlated with tumor size and positively correlated with tumor differentiation in CRC patients. In addition, GLYR1 interacted with MLH1 to regulate its nuclear import and expression. Moreover, downregulation of GLYR1 accelerated G1/S phase transition, promoted proliferation and inhibited differentiation of SW480 and SW620 cells in vitro. Furthermore, downregulation of GLYR1 decreased the sensitivity to 5-fluorouracil (5-FU) by inhibiting the mitochondrial apoptosis pathway in CRC cells. Inhibition of the p38 mitogen-activated protein kinase (p38MAPK) and activation of the phosphatidyl 3-kinase/protein kinase B (PI3K/Akt) signaling pathways were involved in the mechanism by which GLYR1 downregulated p21. Conclusions: Ours is the first study to elucidate the role of GLYR1 in tumors and provide evidence for GLYR1 as a biological marker that reflects the degree of malignancy and sensitivity to 5-FU in MSI CRC.

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“…It has also been reported that the decreased ability of cells to repair DNA caused by GADD45α deletion is highly associated with DNA damage-induced tumorigenesis ( 18 ). In addition, GADD45α has been shown to alleviate multidrug resistance in tumor cells ( 19 ). In one study, the upregulation of GADD45α expression increased the sensitivity of prostate cancer cells to docetaxel ( 20 ).…”

Section: Introductionmentioning

confidence: 99%

GADD45α alleviates the CDDP resistance of SK‑OV3/cddp cells via redox‑mediated DNA damage

et al. 2021

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Epithelial ovarian cancer has the highest mortality rate of all malignant ovarian cancer types. Great progress has been made in the treatment of ovarian cancer in recent years. However, drug resistance has led to a low level of 5-year survival rate of epithelial ovarian cancer, and the molecular mechanism of which remains unknown. The aim of the present study was to identify the role of redox status in the cisplatin (CDDP) resistance of ovarian cancer. CDDP-resistant SK-OV3 (SK-OV3/cddp) cells were prepared and their reactive oxygen species and glutathione levels were investigated. The effects of hydrogen peroxide on the CDDP sensitivity of the SK-OV3/cddp cells and their expression levels of the redox-associated protein growth arrest and DNA damage 45a (GADD45α) were also investigated. In addition, the impact of GADD45α overexpression on cell viability was evaluated in vitro and in vivo, and the levels of Ser-139 phosphorylated H2A histone family member X (γ-H2AX), which is associated with DNA damage, were detected. The results suggested that redox status affected the drug resistance of the ovarian cancer cells by increasing the expression of GADD45α. The overexpression of GADD45α reversed the CDDP resistance of the SK-OV3/cddp cells and increased the level of γ-H2AX. In conclusion, GADD45α alleviated the CDDP resistance of SK-OV3/cddp cells via the induction of redox-mediated DNA damage.

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CtIP promotes G2/M arrest in etoposide‐treated HCT116 cells in a p53‐independent manner

Cited by 7 publications

References 44 publications

MRPL13 Act as a Novel Therapeutic Target and Could Promote Cell Proliferation in Non-Small Cell Lung Cancer

MRPL13 Act as a Novel Therapeutic Target and Could Promote Cell Proliferation in Non-Small Cell Lung Cancer

Downregulation of GLYR1 contributes to microsatellite instability colorectal cancer by targeting p21 via the p38MAPK and PI3K/AKT pathways

GADD45α alleviates the CDDP resistance of SK‑OV3/cddp cells via redox‑mediated DNA damage

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