<scp>MLK</scp>3 silence induces cervical cancer cell apoptosis via the Notch‐1/autophagy network

Ma, Liya; Cheng, Yongchong; Jing, Zeng

doi:10.1111/1440-1681.13123

Cited by 16 publications

(5 citation statements)

References 35 publications

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“…In the cervical cancer microenvironment, many kinds of different moleculars mediate the mutual impact of autophagy and apoptosis. Liya Ma et al performed a study demonstrated that the silence of MLK3 induces the apoptosis of CC cells via the Notch-1/autophagy network [46]. An experiment performed by Liu S et al…”

Section: Discussionmentioning

confidence: 99%

Expression profiling analysis of autophagy-related genes in cervical cancer

Huang

Wang

Liu

et al. 2021

Preprint

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Background: It has been demonstrated by studies globally that autophagy took part in the development of cervical cancer (CC). Few studies concentrated on the correlation between overall survival and CC patients. We retrieved significant autophagy-related genes (ARGs) correlated to the process of cervical cancer. They may be used as prognosis marker or treatment target for clinical application.Methods: Expressions level of genes in cervical cancer and normal tissue samples were obtained from GTEx and TCGA database. Autophagy-related genes (ARGs) were retrieved accroding to the gene list from HaDB. Differentially expressed autophagy related genes (DE-ARGs) related to cervical cancer were identified by Wilcoxon signed-rank test. ClusterProfiler package worked in R software was used to perform GO and KEGG enrichment analyses. Univariate propotional hazard cox regression and multivariate propotional hazard cox regressions were applied to identify DE-ARGs equipped with prognostic value and other clinical independent risk factors. ROC curve was drawn for comparing the survival predict feasibility of risk score with other risk factors in CC patients. Nomogram was drawn to exhibit the prediction model constructed accroding to multivariate cox regression. Correlations between Differentially expressed autophagy related genes (DE-ARGs) and other clinical features were investigated by t test or Cruskal wallis analysis. Correlation between Immune and autophagy in cervical cancer was investigated by ssGSEA and TIMER database. Results: Fifty-six differentially expressed ARGs (DE-ARGs) were retrieved from cervical cancer tissue and normal tissue samples. GO enrichment analysis showed that these ARGs involved in autophagy, ubiquitination of protein and apoptosis. Cox regression medel showed that there were six ARGs significantly associated with overall survival of cervical caner patients. VAMP7 (HR = 0.599, P= 0.033) and TP73 (HR = 0.671, P= 0.014) played protective roles in survival among these six genes. Stage (Stage IV vs Stage I HR = 3.985, P<0.001) and risk score (HR = 1.353, P< 0.001) were sorted as independent prognostic risk factors based on multivariate cox regression. ROC curve validated that risk score was preferable to predict survival of CC patients than other risk factors. Additionally, we found some of these six predictor ARGs were correlated significantly in statistic with tumor grade or stage, clinical T stage, clinical N stage, pathology or risk score (all P< 0.05). The immune cells and immune functions showed a lower activity in high risk group than low risk group which is distincted by median risk score. Conclusion: Our discovery showed that autophagy genes involved in the progress of cervical cancer. Many autophagy-related genes could probably serve as prognostic biomarkers and accelerate the discovery of treatment targets for CC patients.

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Section: Discussionmentioning

confidence: 99%

Expression profiling analysis of autophagy-related genes in cervical cancer

Huang

Wang

Liu

et al. 2021

Preprint

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“…In prostate cancer MLK3 (MAP3K11) also facilitates the collagen type I-induced EMT switch, leading to JNK-mediated increased expression of N-cadherin, an EMT marker associated with promoting migratory and invasive capacity [103,104]. Ma et al [105] showed that MLK3 expression is upregulated in cervical cancer cells and MLK3 blocking suppresses cancer progression via autophagy-dependent apoptosis. Additionally, targeting MAP3K11 using microRNA inhibited tumor proliferation in NSCLC and esophageal cancer [106,107].…”

Section: Map3k11mentioning

confidence: 99%

MAP3K Family Review and Correlations with Patient Survival Outcomes in Various Cancer Types

Nguyen¹,

Tran²,

Rivera³

et al. 2022

Front. Biosci. (Landmark Ed)

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“…7 Cervical cancer (CC) is a malignancy threatening women's reproductive health. 8 So far, a lot of studies have proved that aberrant mRNAs influence CC progression, 9,10 like cell cycle, 11 cell apoptosis, 12 glycolysis, 13 cell autophagy, 14 and epithelial-mesenchymal transition. 15 Therefore, understanding the function of mRNAs in CC progression is of great importance to CC treatment.…”

Section: Introductionmentioning

confidence: 99%

Squalene epoxidase facilitates cervical cancer progression by modulating tumor protein p53 signaling pathway

Guo

Qiao

et al. 2023

J of Obstet and Gynaecol

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Background The mortality of cervical cancer (CC) is quite high and advanced CC is hard to cure. Accordingly, to find the mechanism of CC progression at molecular level is imminent. Methods The mRNA expression data were acquired from The Cancer Genome Atlas database, and squalene epoxidase (SQLE) level in the tumor and adjuvant tissues of CC was analyzed. The pathway enrichment analysis of target mRNAs was performed based on the GSEA database. The cancerous tissues and para‐cancerous tissues of CC patients were collected for immunohistochemistry. SQLE and p53 mRNA expression was ensured by qRT‐polymerase chain reaction. SQLE and p53 protein levels were determined by western blot. Cell functional assays focused on evaluating the malignant behaviors of cancer cells in each treatment group. Nude mouse xenograft models were constructed for tumorigenicity analysis. Results Bioinformatics analysis revealed that SQLE expression was high in CC tissues, which was linked to the poor prognosis. SQLE could affect the p53 signaling pathway. Cell functional assays demonstrated that SQLE expression was promoted in CC cell lines, and overexpressing SQLE facilitated the malignant phenotypes of CC cells, whereas silencing SQLE suppressed CC progression in vitro and in vivo. Besides, the repressed p53 signaling pathway could reverse the effect caused by silenced SQLE. Conclusion SQLE could promote CC progression by modulating the p53 signaling pathway.

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MLK3 silence induces cervical cancer cell apoptosis via the Notch‐1/autophagy network

Cited by 16 publications

References 35 publications

Expression profiling analysis of autophagy-related genes in cervical cancer

Expression profiling analysis of autophagy-related genes in cervical cancer

MAP3K Family Review and Correlations with Patient Survival Outcomes in Various Cancer Types

Squalene epoxidase facilitates cervical cancer progression by modulating tumor protein p53 signaling pathway

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