miR-106a suppresses tumor cells death in colorectal cancer through targeting ATG7

Hao, Haibin; Xia, Guangfeng; Wang, Chao; Zhong, Fangchuan; Liu, Laipeng; Zhang, Dong

doi:10.1007/s00795-016-0150-7

Cited by 41 publications

(25 citation statements)

References 24 publications

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“…MiR-106a was also indicated to suppress tumor cells death in colorectal cancer. 21 However, enforced expression of miR-106a in gastric cancer could promote tumor metastasis. 23 Although the effects of miR-106a on cancers were controversial, our findings were in accordance with previous reports, in which miR-106a was identified as a therapeutic biomarker for DKD and showed beneficial effect in HG-induced injury.…”

Section: Discussionmentioning

confidence: 99%

<p>LncRNA SNHG16 Aggravates High Glucose-Induced Podocytes Injury in Diabetic Nephropathy Through Targeting miR-106a and Thereby Up-Regulating KLF9</p>

Zeng

2020

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Introduction Diabetic nephropathy (DN) is one of the major complications of diabetes and podocyte injury plays an important role in the DN pathogenesis. MicroRNA (miR)-106a is predicated to be a target of long noncoding RNA (lncRNA) SNHG16 and has been identified as a therapeutic biomarker for diabetic kidney diseases. However, the role of SNHG16/miR-106a axis in DN has not been illustrated. This study aimed to investigate whether SNHG16 could regulate podocyte injury via miR-106a in DN and uncover the underlying mechanism. Methods MPC5 podocytes were treated with control or high glucose (HG) medium, and then miR-106a level was measured. MPC5 cells that exposed to HG were overexpressed with miR-106a or not, following by overexpression with or without KLF9 or SNHG16. Then, cell viability, apoptosis, reactive oxygen species and the protein expression of synaptopodin and podocin were evaluated. Results MiR-106a was down-regulated in the serum of DN patients and HG-induced MPC5 podocytes. Overexpression of miR-106a suppressed HG-induced decrease in cell viability, Bcl-2, synaptopodin and podocin expression, increase in ROS, apoptotic cells, Bax and cleaved-caspase 3 expression. MiR-106a could bind to both KLF9 and lncRNA SNHG16, which were up-regulated in the serum of DN patients and HG-induced MPC5 podocytes. The level of miR-106a was decreased by SNHG16 overexpression and miR-106a overexpression reduced KLF9 expression. Furthermore, overexpression of KLF9 or SNHG16 blunted the protective effects of miR-106a on HG-induced MPC5 injury. Discussion LncRNA SNHG16 could promote HG-stimulated podocytes injury via targeting miR-106a to enhance KLF9 expression. The intervention of SNHG16/miR-106a/KLF9 may be a therapeutic treatment for DN.

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Section: Discussionmentioning

confidence: 99%

<p>LncRNA SNHG16 Aggravates High Glucose-Induced Podocytes Injury in Diabetic Nephropathy Through Targeting miR-106a and Thereby Up-Regulating KLF9</p>

Zeng

2020

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“…1, on the basis of initial literature research, a total of 225 qualified articles were involved from the selected databases. According to the inclusion and exclusion criteria, after removing the duplicates and reviewing the texts, 19 articles including 28 studies were utilized for the final analysis, of which 6 studies were about the value of miR-106 family for CRC diagnosis and 22 studies were about CRC prognosis [8,[20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35][36]. All studies applied quantitative reverse transcription PCR (qRT-PCR) to measure the expression of miR-106…”

Section: Literature Search and Demographic Characteristicsmentioning

confidence: 99%

Biomarker roles identification of miR-106 family for predicting the risk and poor survival of colorectal cancer

et al. 2020

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Background: Recent studies have extensively investigated the roles of miR-106 in colorectal cancer (CRC). However, the associations and molecular mechanism underlying the roles of miR-106 in CRC remain unclear. We aimed to thoroughly investigate the biomarker roles of miR-106 for predicting the risk and survival outcome in CRC. Methods: We first conducted a comprehensive meta-analysis to quantitatively evaluate the roles of miR-106 in the diagnosis and prognosis of CRC. Then, we qualitatively explored the biomarker roles of miR-106 in CRC through an integrative bioinformatics analysis. Results: The results indicated that miR-106 yielded a combined AUC of 0.79 (95% CI: 0.76-0.83), with a pooled sensitivity of 0.50 (95% CI: 0.32-0.68) and a pooled specificity of 0.93 (95% CI: 0.79-0.98) for discriminating CRC cases from normal controls. Moreover, patients with higher expression of miR-106 were significantly associated with shorter disease-free survival (HR: 1.73; 95%CI: 1.23-2.44) and overall survival (HR: 1.39; 95%CI: 1.09-1.77). Finally, gene ontology and pathway analysis demonstrated that miR-106 family was highly involved in the initiation and progression of CRC and indicated the potential molecular mechanism for miR-106 in CRC. Conclusions: Our results indicated that miR-106 showed promising potential as diagnostic and prognostic biomarker for CRC. Nevertheless, the underlying molecular mechanism of miR-106 family involved in CRC requires further investigation.

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“…Autophagy genes are the key components of the autophagymediated regulatory network. They are implicated in the occurrence and development of CRC (Hao et al, 2017). We have systematically validated the autophagy genes of differential expression, through data comparison of diverse stages for CRC.…”

Section: Discussionmentioning

confidence: 99%

“…However, this observation should be interpreted with caution, because there are many uncertainties in the upstream regulatory factors of autophagy. Alterations in various molecular levels could cause expression dysregulation of autophagy genes (Hao et al, 2017). Therefore, further efforts are required to elucidate the corresponding contributions of various factors in the expression signatures of the autophagy gene of CRC (Wang et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Identification of Autophagy-Associated Biomarkers and Corresponding Regulatory Factors in the Progression of Colorectal Cancer

et al. 2020

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Autophagy is a self-degradation process that maintains homeostasis against stress in cells. Autophagy dysfunction plays a central role in the development of tumors, such as colorectal cancer (CRC). In this study, autophagy-related differentially expressed genes, their downstream functions, and upstream regulatory factors including RNAbinding proteins (RBP) involved in programmed cell death in the CRC were investigated. Transcription factors (TFs) and miRNAs have been shown to mainly regulate autophagy genes. Interestingly, we found that some of the RBP in the CRC, such as DDX17, SETDB1, and POLR3A, play an important regulatory role in maintaining autophagy at a basal level during growth by acting as TFs that regulate autophagy. Promoter methylations showed negative regulations on differentially expressed autophagy gene (DEAG), while copy number variations revealed a positive role in them. A proportional hazards regression analysis indicated that using autophagy-related prognostic signature can divide patients into high-risk and low-risk groups. Autophagy associated FDAapproved drugs were studied by a prognostic network. This would contribute to the identifications of new potential molecular therapeutic targets for CRC.The relationship between DEAGs expression level and patient survival was evaluated by the Cox regression analysis. Multivariate Cox regression analysis was used to fit the selected 2 www.broadinstitute.org/ccle 3

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miR-106a suppresses tumor cells death in colorectal cancer through targeting ATG7

Cited by 41 publications

References 24 publications

<p>LncRNA SNHG16 Aggravates High Glucose-Induced Podocytes Injury in Diabetic Nephropathy Through Targeting miR-106a and Thereby Up-Regulating KLF9</p>

<p>LncRNA SNHG16 Aggravates High Glucose-Induced Podocytes Injury in Diabetic Nephropathy Through Targeting miR-106a and Thereby Up-Regulating KLF9</p>

Biomarker roles identification of miR-106 family for predicting the risk and poor survival of colorectal cancer

Identification of Autophagy-Associated Biomarkers and Corresponding Regulatory Factors in the Progression of Colorectal Cancer

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