PGAM1, regulated by miR-3614-5p, functions as an oncogene by activating transforming growth factor-β (TGF-β) signaling in the progression of non-small cell lung carcinoma

Li, Fangfang; Yang, Hao; Kong, Tiandong; Chen, Shanshan; Li, Ping; Chen, Lu; Cheng, Jiuling; Cui, Guangying; Zhang, Guojun

doi:10.1038/s41419-020-02900-4

Cited by 29 publications

(27 citation statements)

References 29 publications

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“…MiR-3614-5p displayed low expression in HCC tissues and cells and overexpression of miR-3614-5p totally reversed the inhibitory effect of LOXL1-AS1 knockdown on HCC cell malignant behaviors. It has been reported that miR-3614-5p could repress cell proliferation and invasion of non-small cell lung cancer [ 33 ], which further supported the anti-tumor role of miR-3614-5p in HCC cells.…”

Section: Discussionmentioning

confidence: 60%

Study on the mechanism of LOXL1-AS1/miR-3614-5p/YY1 signal axis in the malignant phenotype regulation of hepatocellular carcinoma

Feng

Xie

et al. 2021

Biol Direct

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Background Hepatocellular carcinoma (HCC) is one of the most common malignant tumors with high mortality worldwide. Accumulating researches have indicated that long non‑coding RNAs (lncRNAs) are involved in varies human cancers, including HCC. Nevertheless, the specific molecular mechanism of lncRNA lysyl oxidase like 1 antisense RNA 1 (LOXL1-AS1) in HCC is still unclear. Methods LOXL1-AS1 expression was tested via qRT-PCR in HCC cells. Functional and mechanism assays were respectively done to evaluate the biological functions of HCC cells and the potential interaction of LOXL1-AS1 and other factors. Results We discovered that LOXL1-AS1 was high expressed in HCC cells. Inhibition of LOXL1-AS1 repressed cell proliferation, migration and invasion, but enhanced cell apoptosis in HCC. Further, miR-3614-5p was proven to be sponged by LOXL1-AS1. Additionally, Yin Yang 1 (YY1) was proven as the target gene of miR-3614-5p, and YY1 depletion could repress HCC cell malignant behaviors. YY1 could also transcriptionally activate LOXL1-AS1 expression. In rescue assays, we confirmed that overexpression of YY1 or miR-3614-5p inhibition could reverse the suppressive effects of LOXL1-AS1 silence on the malignant behaviors of HCC cells. Conclusion In short, LOXL1-AS1/miR-3614-5p/YY1 forms a positive loop in modulating HCC cell malignant behaviors.

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Section: Discussionmentioning

confidence: 60%

Study on the mechanism of LOXL1-AS1/miR-3614-5p/YY1 signal axis in the malignant phenotype regulation of hepatocellular carcinoma

Feng

Xie

et al. 2021

Biol Direct

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“…Tumortargeted glycolysis is considered a potential therapeutic strategy for tumor targeting. PGAM1 is a key enzyme for glycolysis, and a large number of studies suggest that PGAM1 is closely related to the malignant progression of tumors [10][11][12][13]. However, whether PGAM1 has a regulatory role in breast cancer remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Expression and Gene Regulation Network of Metabolic Enzyme Phosphoglycerate Mutase Enzyme 1 in Breast Cancer Based on Data Mining

Wang

Xiong

Hua

et al. 2021

BioMed Research International

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The metabolic enzyme phosphoglycerate mutase enzyme 1 (PGAM1) is a key enzyme in the glycolysis pathway, and glycolysis is closely related to cancer progression, suggesting that PGAM1 may have important functions in breast cancer. We used sequencing data from the Oncomine database and UALCAN database to analyze the expression of PGAM1 and its influence on the clinicopathological characteristics of breast cancer. LinkedOmics was used to identify genes related to PGAM1 expression, kinases, miRNAs, and transcription factors that were significantly related to PGAM1 through GSEA. cBioPortal was used to identify the alternation frequency and form of PGAM1 in breast cancer. The expression level of PGAM1 in breast cancer was significantly higher than that in normal tissues. Moreover, the expression level of PGAM1 is closely related to the molecular subtype and TP53 mutation status. The expression level of PGAM1 in HER2-positive and triple-negative tumors was significantly higher than that of luminal type. The expression level of PGAM1 in TP53-mutant tumors was higher than that in non-TP53-mutant tumors. In addition, the overall survival of patients with high PGAM1 expression was significantly worse than that of patients with low expression ( P = 0.0077 ). Through GSEA analysis, we found multiple kinases, miRNAs, and transcription factors significantly related to PFKFB4. cBioPortal analysis showed that the mutation rate of PGAM1 in breast cancer was relatively low (4%), and the main form of mutation was high mRNA expression. This study suggests that PGAM1 is a potential diagnostic and prognostic marker in breast cancer. Through data mining, we revealed the potential regulatory network information of PGAM1, laying a foundation for further research on the role of PGAM1 in breast cancer.

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“…13 PGAM1 is highly expressed in various tumors, such as oral squamous cell carcinoma, prostate cancer, non-small cell lung cancer, renal clear cell carcinoma, pancreatic ductal carcinoma, and colorectal cancer, and is associated with tumor invasion, migration, and proliferation. [14][15][16][17][18][19] The present study showed that ENO1 and PGAM1 are highly expressed in MM. Understanding the cooperative mechanism by which ENO1 and PGAM1 affect MM development is our next research direction.…”

Section: Discussionmentioning

confidence: 92%

ENO1 Inhibits Apoptosis and Promotes Cell Invasion and Proliferation in Malignant Melanoma

Zhang

Tian

Zhang

et al. 2021

Preprint

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Introduction The glycolytic enzyme, α-Enolase (ENO1), catalyzes the production of phosphoenolpyruvate from 2-phosphoglycerate, which enhances glycolysis, and thus contributes to tumor progression. In the present study, we aimed to determine ENO1’s role in malignant melanoma (MM) and the potential underlying mechanism. Methods Western blotting was used to assess the levels of ENO1, c-Myc, β-catenin, MMP-9, PGAM1, and MMP-13 in MM-derived cell lines or tumor tissues from patients with MM. Plasmids pCMV-SPORT6-ENO1 and pET-28a-ENO1siRNA plasmids were used to overexpress and knockdown ENO1 in MM cells, respectively. To determine the function of ENO1 in the malignant behavior of MM cells, we performed wound healing, Cell counting kit 8, Transwell chamber, and flow cytometry analyses. Pyruvate determination and lactic acid kits were used to evaluate the production of pyruvate and lactic acid in tumor cells. Results The protein levels of ENO1 and PGAM1 in MM tissue were significantly higher than that in mole tissue. In MM cells, ENO1 overexpression inhibited apoptosis; promoted invasion, migration, and proliferation; increased pyruvate and lactate production; and increased in β-catenin, MMP-9, MMP-13, and c-Myc levels. The opposite effects were observed in MM cells silenced for ENO1. Conclusion These results indicated that ENO1 is involved in MM progression by enhancing invasion and proliferation, while inhibiting apoptosis. In addition, ENO1 might have an important function in tumor cell glycolysis. Therefore, ENO1 represents a potential therapeutic target to treat MM.

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PGAM1, regulated by miR-3614-5p, functions as an oncogene by activating transforming growth factor-β (TGF-β) signaling in the progression of non-small cell lung carcinoma

Cited by 29 publications

References 29 publications

Study on the mechanism of LOXL1-AS1/miR-3614-5p/YY1 signal axis in the malignant phenotype regulation of hepatocellular carcinoma

Study on the mechanism of LOXL1-AS1/miR-3614-5p/YY1 signal axis in the malignant phenotype regulation of hepatocellular carcinoma

Expression and Gene Regulation Network of Metabolic Enzyme Phosphoglycerate Mutase Enzyme 1 in Breast Cancer Based on Data Mining

ENO1 Inhibits Apoptosis and Promotes Cell Invasion and Proliferation in Malignant Melanoma

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