Long non-coding RNA MSC-AS1 facilitates the proliferation and glycolysis of gastric cancer cells by regulating PFKFB3 expression

Jin, Xianzhen; Qiao, Liang; Fan, Hui; Liao, Chunyan; Zheng, Jianbao; Wang, Wei; Ma, Xiuqin; Yang, Min; Sun, Xuejun; Zhao, Wei

doi:10.7150/ijms.51947

Cited by 21 publications

(17 citation statements)

References 36 publications

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“…The human gastric cancer cell lines, AGS, SGC-7901, MGC-803, and MKN-45, and the gastric mucosal cell line, GES-1, were maintained and cultured under standard conditions in our lab 21 . The expression vectors, PSMD7-OE and RAD23B-OE, were constructed by inserting the cDNA products of PSMD7 and RAD23B into the pcDNA3.1(+) vector (V79020, Invitrogen, Carlsbad, CA, USA) and transfected into GC cells using Effectene transfection reagent (301427, Qiagen, Valencia, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

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Deubiquitinase PSMD7 promotes the proliferation, invasion, and cisplatin resistance of gastric cancer cells by stabilizing RAD23B

Wang¹,

Liu²,

Mo³

et al. 2021

Int. J. Biol. Sci.

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Ubiquitination, a crucial post-translational modification, controls substrate degradation and can be reversed by deubiquitinases (DUBs). An increasing number of studies are showing that DUBs regulate the malignant behavior and chemotherapy resistance of gastric cancer (GC) by stabilizing various proteins. However, the expression level and biological function of the DUB, proteasome 26S subunit, non-ATPase 7 (PSMD7), in GC remains unknown. Herein, we report for the first time that PSMD7 is frequently overexpressed in GC tissues. Elevated levels of PSMD7 were also detected in GC cell lines. Notably, the upregulation of PSMD7 closely correlated with malignant clinical parameters and reduced the survival of GC patients. Functionally, we found that PSMD7 knockdown consistently suppressed the proliferation, migration, and invasion of AGS and SGC-7901 cells. Ectopic expression of PSMD7 facilitated GC cell proliferation and mobility. Based on protein-protein interaction prediction, RAD23 homolog B (RAD23B) protein was identified as a candidate substrate of PSMD7. PSMD7 positively regulated the abundance of RAD23B and xeroderma pigmentosum, complementation group C (XPC) protein in GC cells. The interaction between PSMD7 and RAD23B was confirmed using protein immunoprecipitation. PSMD7 knockdown enhanced the ubiquitination and degradation of RAD23B protein in GC cells. PSMD7 promoted cell viability, apoptosis resistance, and DNA damage repair in GC cells upon cisplatin (DDP) treatment. Moreover, PSMD7 silencing inhibited tumor growth and enhanced the sensitivity of GC cells to DDP treatment in mice. In summary, PSMD7 was highly expressed in GC and contributed to the malignant behavior and DDP resistance of tumor cells by stabilizing RAD23B.

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Section: Methodsmentioning

confidence: 99%

“…The proliferation of GC cells was assessed using the thiazolyl blue tetrazolium bromide (MTT) assay with the MTT reagent (CT02, Sigma-Aldrich) and the 5-ethynyl-2′-deoxyuridine (EdU) assay with the Cell-Light™ EdU Apollo®488 In vitro Imaging Kit (C10310-1, RiboBio, Guangzhou, China), as previously described 21 .…”

Section: Methodsmentioning

confidence: 99%

Deubiquitinase PSMD7 promotes the proliferation, invasion, and cisplatin resistance of gastric cancer cells by stabilizing RAD23B

Wang¹,

Liu²,

Mo³

et al. 2021

Int. J. Biol. Sci.

Self Cite

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“…MSC-AS1 induces PGK1 expression and accelerates the progression of HCC ( 30 ). In addition, MSC-AS1 has a similar role in gliomas ( 31 ), gastric cancer ( 32 ), renal clear cell carcinoma ( 33 ), and pancreatic cancer ( 34 ). TMEM220-AS1, AC015908.3, AC009005.1, and AL031985.3 have been reported in a signature predictive of overall survival.…”

Section: Discussionmentioning

confidence: 99%

A Novel Nine-lncRNA Risk Signature Correlates With Immunotherapy in Hepatocellular Carcinoma

Nie

et al. 2021

Front. Oncol.

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BackgroundHepatocellular carcinoma is one of the most common malignant tumors with a very high mortality rate. The emergence of immunotherapy has brought hope for the cure of hepatocellular carcinoma. Only a small number of patients respond to immune checkpoint inhibitors, and ferroptosis and tertiary lymphoid structure contribute to the increased response rate of immune checkpoint inhibitors; thus, we first need to identify those who are sensitive to immunotherapy and then develop different methods to improve sensitivity for different groups.MethodsThe sequencing data of hepatocellular carcinoma from The Cancer Genome Atlas and Gene Expression Omnibus was downloaded to identify the immune-related long non-coding RNAs (lncRNAs). LncRNAs related to survival data were screened out, and a risk signature was established using Cox proportional hazard regression model. R software was used to calculate the riskScore of each patient, and the patients were divided into high- and low-risk groups. The prognostic value of riskScore and its application in clinical chemotherapeutic drugs were confirmed. The relationship between riskScore and immune checkpoint genes, ferroptosis genes, and genes related to tertiary lymphoid structure formation was analyzed by Spearman method. TIMER, CIBERSORT, ssGSEA, and ImmuCellAI were used to evaluate the relative number of lymphocytes in tumor. The Wilcoxon signed-rank test confirmed differences in immunophenoscore between the high- and low-risk groups.ResultsData analysis revealed that our signature could well predict the 1-, 2-, 3-, and 5-year survival rates of hepatocellular carcinoma and to predict susceptible populations with Sorafenib. The risk signature were significantly correlated with immune checkpoint genes, ferroptosis genes, and tertiary lymphoid structure-forming genes, and predicted tumor-infiltrating lymphocyte status. There was a significant difference in IPS scores between the low-risk group and the high-risk group, while the low-risk group had higher scores.ConclusionThe riskScore obtained from an immune-related lncRNA signature could successfully predict the survival time and reflect the efficacy of immune checkpoint inhibitors. More importantly, it is possible to select different treatments for different hepatocellular carcinoma patients that increase the response rate of immune checkpoint inhibitors and will help improve the individualized treatment of hepatocellular carcinoma.

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“…Linc-00475 also affects cancer progression via glycolysis. Jin et al have found that Linc-MSC-AS1 promotes the proliferation and glycolysis of gastric cancer cells by regulating the expression of PFKFB3 [20]. The study by Du et al has found that Linc-MIR210HG promotes aerobic glycolysis by regulating the expression of HIF-1α, which leads to the progression of triple-negative breast cancer [21].…”

Section: Discussionmentioning

confidence: 99%

Effect of Linc-00475 Regulation of p53 on Glycolysis and Survival in Gastric Cancer

Zhang

Wang

2021

Preprint

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Background: Abnormal glucose metabolism leading to tumor proliferation and metastasis is an important area of interest in cancer treatment. The purpose of this study was to investigate the effects of clinical expression of glucose metabolism-related genes Linc-00475 and p53 on glycolysis and survival.Methods: A key differential gene Linc-00475 was screened using a metabolic database, and its downstream gene, p53, was predicted. A total of 107 gastric cancer tissue samples from patients diagnosed at our center between 2011 and 2013 were selected. The expression levels of Linc-00475 and p53 were detected via in situ hybridization or immunohistochemistry. Chi-square test was used to analyze the relationship between Linc-00475 and p53 expression and clinicopathological factors. Kaplan-Meier method and log rank test were used to analyze patients’ overall survival. To determine the effect of Linc-00475 on glycolysis, qRT-PCR and western blot were utilized to evaluate the regulatory relationship between Linc-00475 and p53.Results: High expression of Linc-00475 (P < 0.001) and low expression of p53 (P < 0.01) were associated with poor prognosis. There was a negative correlation between the expression of Linc-00475 and p53 in gastric cancer (Pearson's coefficient test, r = -0.405; P < 0.001). The co-expression of high-level Linc-00475 and low-level p53 can thus be used as an independent prognostic factor (P = 0.001). Linc-00475 was also shown to regulate aerobic glycolysis. Western blot and qRT-PCR demonstrated that Linc-00475 regulates the expression of p53.Conclusion: The co-expression of Linc-00475 and p53 can be used as a reference index for evaluating the prognosis of gastric cancer. Linc-00475 regulates p53, thereby affecting glycolysis.

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Long non-coding RNA MSC-AS1 facilitates the proliferation and glycolysis of gastric cancer cells by regulating PFKFB3 expression

Cited by 21 publications

References 36 publications

Deubiquitinase PSMD7 promotes the proliferation, invasion, and cisplatin resistance of gastric cancer cells by stabilizing RAD23B

Deubiquitinase PSMD7 promotes the proliferation, invasion, and cisplatin resistance of gastric cancer cells by stabilizing RAD23B

A Novel Nine-lncRNA Risk Signature Correlates With Immunotherapy in Hepatocellular Carcinoma

Effect of Linc-00475 Regulation of p53 on Glycolysis and Survival in Gastric Cancer

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