Micro<scp>RNA</scp>‐33a‐5p suppresses colorectal cancer cell growth by inhibiting <scp>MTHFD</scp>2

Yan, Yan; Zhang, Ding; Lei, Ting; Zhao, Chuanqi; Han, Jing; Cui, Jiarui; Wang, Yili

doi:10.1111/1440-1681.13125

Cited by 28 publications

(26 citation statements)

References 26 publications

(30 reference statements)

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“…14 Yan et al revealed that miR-33a-5p repressed cell proliferation and migratory abilities in colorectal cancer. 30 Besides, miR-33a-5p was demonstrated to suppress cell proliferation and metastasis in hepatocellular carcinoma. 31 In consistent with their finding, our results explained miR-33a-5p overexpression abolished the effects of circ_ASAP2 on GC progression, and this meant that miR-33a-5p inhibited GC progression.…”

Section: Discussionmentioning

confidence: 99%

<p>Gambogic Acid Inhibits the Progression of Gastric Cancer via circRNA_ASAP2/miR-33a-5p/CDK7 Axis</p>

Lin¹,

Lin²,

He³

et al. 2020

CMAR

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Background: Gastric cancer (GC) is a major cancer-related mortality disease. Gambogic acid (GA) has been investigated to inhibit cancer progression. In the present study, the molecular mechanism of GA in regulating GC progression was studied. Methods: The expression levels of circular RNA ASAP2 (circ_ASAP2), miR-33a-5p and cyclin-dependent kinases 7 (CDK7) were detected by quantitative real-time polymerase reaction (qRT-PCR). CDK7 protein level was evaluated by Western blot. Cell colony formation assay, 3-(4,5-Dimethylthazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, transwell assay and flow cytometry analysis were employed to reveal the functional effects among circ_ASAP2, miR-33a-5p and CDK7 on GA-induced GC progression. Mechanistically, the binding relationship between miR-33a-5p and circ_ASAP2 or CDK7 was predicted with starBase v3.0 online database and verified by dual-luciferase reporter assay. In vivo tumor formation assay was used to explain the impacts of GA treatment on GC growth in vivo. Results: Circ_ASAP2 and CDK7 expression were downregulated in GA-induced GC cells compared with GC cells. MiR-33a-5p expression was upregulated in GA-induced GC cells relative to GC cells. The protein expression level of CDK7 was lower in GA-induced GC cells than that in GC cells. Further, circ_ASAP2 overexpression decreased GA-induced inhibition effects on cell proliferation, migration and invasion and GA-induced promotion effect on cell apoptosis in both AGS and HGC-27 cells, whereas this phenomenon was reversed by miR-33a-5p. In addition, circ_ASAP2 functioned as a sponge of miR-33a-5p and miR-33a-5p was associated with CDK7. Furthermore, GA treatment inhibited GC growth in vivo. Conclusion: Circ_ASAP2 overexpression promoted cell proliferation, migration and invasion, whereas inhibited cell apoptosis by upregulating CDK7 expression through binding to miR-33a-5p in GA-induced GC cells. This study provided a theoretical basis in GC treatment with GA.

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Section: Discussionmentioning

confidence: 99%

<p>Gambogic Acid Inhibits the Progression of Gastric Cancer via circRNA_ASAP2/miR-33a-5p/CDK7 Axis</p>

Lin¹,

Lin²,

He³

et al. 2020

CMAR

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“…In colorectal cancer, MTHFD2 expression promotes cancer cell growth, and MTHFD2 is targeted by miR-33a-5p, a microRNA with a major role in tumorigenesis. [ 32 ] In addition, miR-92a inhibits cancer cell proliferation and induces apoptosis by regulating MTHFD2 in acute myeloid leukemia. [ 33 ] Similarly, miR-9 can directly target MTHFD2 to exert anti-proliferative and pro-apoptotic effects in breast cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Identification of MTHFD2 as a novel prognosis biomarker in esophageal carcinoma patients based on transcriptomic data and methylation profiling

et al. 2020

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DNA methylation is an important epigenetic regulatory mechanism in esophageal carcinoma (EC) and is associated with genomic instability and carcinogenesis. In the present study, we aimed to identify tumor biomarkers for predicting prognosis of EC patients. We downloaded mRNA expression profiles and DNA methylation profiles associated with EC from the Gene Expression Omnibus database. Differentially expressed and differentially methylated genes between tumor tissues and adjacent normal tissue samples were identified. Functional enrichment analyses were performed, followed by the construction of protein–protein interaction networks. Data were validated based on methylation profiles from The Cancer Genome Atlas. Candidate genes were further verified according to survival analysis and Cox regression analysis. We uncovered multiple genes with differential expression or methylation in tumor samples compared with normal samples. After taking the intersection of 3 differential gene sets, we obtained a total of 232 overlapping genes. Functional enrichment analysis revealed that these genes are related to pathways such as “glutathione metabolism,” “p53 signaling pathway,” and “focal adhesion.” Furthermore, 8 hub genes with inversed expression and methylation correlation were identified as candidate genes. The abnormal expression levels of MSN, PELI1, and MTHFD2 were correlated with overall survival times in EC patients ( P < .05). Only MTHFD2 was significantly associated with a pathologic stage according to univariate analysis ( P = .037) and multivariate analysis ( P = .043). Our study identified several novel EC biomarkers with prognostic value by integrated analysis of transcriptomic data and methylation profiles. MTHFD2 could serve as an independent biomarker for predicting prognosis and pathological stages of EC.

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“…Xu et, al suggested that microRNA-940 could inhibit glioma progression by blocking mitochondrial folate metabolism through targeting of MTHFD2 [31]. Yam et, al indicated that microRNA-33a-5p suppresses the growth and migration of colorectal cancer cell by inhibiting MTHFD2 [32]. Li et, al reported that upregulation of miR-504-3p is associated with favorable prognosis of acute myeloid leukemia and may serve as a tumor suppressor by targeting MTHFD2 [33].…”

Section: Discussionmentioning

confidence: 99%

Up-regulated Expression of MTHFD2 Correlates with Favorable Prognosis in LGG Patients: A Bioinformatic Analysis

Shi¹,

Zhang²,

Shou³

et al. 2020

Preprint

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Background Methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) was found to be up-regulated in various cancers and has been identified as a potential target for cancer treatment, but the potential function of MTHFD2 in low-grade gliomas (LGG) has not been well-examined. This study initially revealed the potential function of MTHD2 and emphasized its importance in LGG. Methods We first explored the expression of MTHFD2 in LGG patients using Oncomine and UALCAN database. Survival analysis on LGG patients was then conducted based on age, gender, radiation therapy, histologic grade, tumor type and MTHFD2 expression. Cox regression analysis was also applied to predict the prognostic factor for overall survival (OS) of LGG. Finally, we performed enrichment analysis to reveal the potential MTHFD2-associated pathways involved in LGG. Results We found that MTHFD2 is highly expressed in LGG patients, and MTHFD2 expression is related with age, sub-types and TP53-mutation status (all P<0.05). Age, radiation therapy, histologic grade and tumor type were implicated in the survival of LGG patients (all P<0.05). High expression of MTHFD2 desirably improved the prognosis of LGG patients (P<0.001), especially for those patients with characteristics of age≥45 years old (P<0.001), receiving radiation therapy treatment (P=0.001), sub-type of astrocytoma and oligodendroglioma (all P<0.05), and histologic grade 3 (P<0.05). MTHFD2 was determined as an independent prognostic factor with age and grade for OS of LGG patients (all P<0.01). Pathway enrichment analysis indicated that MTHFD2 mainly participates in mTOR signaling pathway, apelin pathway and folate-mediated one-carbon metabolism.Conclusions The expression of MTHFD2 is associated with key clinical phenotype. High expression of MTHFD2 is favorable for the overall survival of LGG patients. MTHFD2 may serve as a novel prognostic biomarker and potential therapeutic target for LGG treatment.

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MicroRNA‐33a‐5p suppresses colorectal cancer cell growth by inhibiting MTHFD2

Cited by 28 publications

References 26 publications

<p>Gambogic Acid Inhibits the Progression of Gastric Cancer via circRNA_ASAP2/miR-33a-5p/CDK7 Axis</p>

<p>Gambogic Acid Inhibits the Progression of Gastric Cancer via circRNA_ASAP2/miR-33a-5p/CDK7 Axis</p>

Identification of MTHFD2 as a novel prognosis biomarker in esophageal carcinoma patients based on transcriptomic data and methylation profiling

Up-regulated Expression of MTHFD2 Correlates with Favorable Prognosis in LGG Patients: A Bioinformatic Analysis

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