Upregulation of miR‐675‐5p induced by lncRNA H19 was associated with tumor progression and development by targeting tumor suppressor p53 in non–small cell lung cancer

Zheng, Zihui; Wu, Dongmei; Fan, Shao‐Hua; Zhang, Zi‐Feng; Chen, Gui‐Quan; Lü, Jun

doi:10.1002/jcb.29182

Cited by 55 publications

(48 citation statements)

References 39 publications

(78 reference statements)

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“…The competing endogenous (ce)RNA hypothesis suggests that the expression of lncRNAs controls the mRNAs levels via sponging miRNAs (14). Several lncRNAs have been reported to be oncogenes or tumor suppressors in NSCLC (15)(16)(17). For instance, Yang et al (18) indicated that lncRNA insulin-like growth factor binding protein 4-1 was significantly upregulated in lung cancer and promoted tumor cell metabolism to facilitate cancer cell proliferation.…”

Section: Introductionmentioning

confidence: 99%

lncRNA TPTEP1 competitively sponges miR‑328‑5p to inhibit the proliferation of non‑small cell lung cancer cells

Cao

Wang²,

Feng

et al. 2020

Oncol Rep

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Accumulating evidence suggests that lncRNAs are involved in almost all normal physiological processes and that aberrant expression of lncRNAs may be involved in the development of diseases, including non-small cell lung cancer (NSCLC). However, the roles of lncRNA-TPTE pseudogene 1 (TPTEP1) in lung cancer and the underlying molecular mechanisms have remained elusive. In the present study, significant downregulation of TPTEP1 in tumors compared with normal tissues from patients with NSCLC was observed. Overexpression of TPTEP1 inhibited cell proliferation and induced apoptosis in NSCLC cells. A bioinformatics analysis based on miRDB predicted microRNA (miR)-328-5p as a potential binding miRNA for TPTEP1. Using a dual-luciferase reporter assay and western blot analysis, it was further validated that TPTEP1 sponged miR-328-5p to upregulate Src kinase signaling inhibitor 1 (SRCIN1) in NSCLC cells. Through regulation of SRCIN1, TPTEP1 was indicated to inactivate the Src and STAT3 pathways in NSCLC cells. Notably, silencing of SRCIN1 reversed the TPTEP1 overexpression-induced inhibition of cell proliferation and increase of the apoptotic rate in NSCLC cells. Pearson correlation analysis revealed a significant positive correlation between TPTEP1 and SRCIN1 mRNA levels in NSCLC tumors. The present results provided insight into the roles of TPTEP1 in NSCLC and the underlying mechanisms.

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Section: Introductionmentioning

confidence: 99%

lncRNA TPTEP1 competitively sponges miR‑328‑5p to inhibit the proliferation of non‑small cell lung cancer cells

Cao

Wang²,

Feng

et al. 2020

Oncol Rep

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“…There is evidence that reduced H19 and miR675 expression led to increased p53 protein expression, which regulates cell apoptosis [25]. Our data showed that mutation of the regions upstream of the m 6 A modification site inhibited miR675 and H19 expression, inducing cell apoptosis, possibly through the p53 protein.…”

Section: Discussionmentioning

confidence: 52%

Targeted point mutations of the m6A modification in miR675 using RNA-guided base editing induce cell apoptosis

Hao

Lin

et al. 2020

Bioscience Reports

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Methylation of the adenine base at the nitrogen 6 position (m6A) is the most common post-transcriptional epigenetic modification of RNA, and it plays a very important role in regulating gene expression. To investigate the role of m6A methylation in the expression of non-coding RNA and miRNA, we used a system of adenine base editors (ABEs). Here, we mutated regions up- and downstream of miRNA 675 m6A modification sites in the H19 locus using HEK293T, L02, MHCC97L, MHCC97H, A549, and SGC-7901 cells. Our results showed that a T–A base transversion had occurred in all cell lines. Moreover, mutation of the regions upstream of the miRNA 675 m6A modification site led to reduced expression of H19 and the induction of cell apoptosis in HEK293T cells. To further confirm our results, L02 and MHCC97L cells were detected using ABEs system. The results indicated increased cell apoptosis and reduced expression of miR675 as well as H19. To confirm the relationship between H19 and miR675 expression, overexpression and knockdown studies were performed. The results showed that reduced HI9 expression induced cell apoptosis through miR675. Taken together, these results indicate that m6A modification can regulate the expression of H19 and miR675 which induce cell apoptosis.

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“…So far, 10 polymorphisms in H19 have been identi ed as predisposing factors to various cancer types, among which the rs217727 has been most frequently studied, followed by rs2839698 [45]. H19 plays an essential role in the tumor progression of breast cancer [15], bladder cancer [46], gastric cancer [17], and other tumors [20,47,48], other than that, mutations in the H19 gene coding sequence are also closely related to tumors, despite unknown regulatory mechanisms [12,49]. The following evidence suggests that SNPs may affect the expression and function of the H19 gene.…”

Section: Discussionmentioning

confidence: 99%

“…More and more evidence indicates that the H19 gene is essential for human tumor growth from different biological processes [15]. Studies have shown that the H19 gene was upregulated in lung cancer, gastric cancer, colon cancer, retinoblastoma, thyroid cancer and breast cancer [15][16][17][18][19][20]. However, the up-regulated expression of the H19 gene can inhibit pituitary tumor cell proliferation in vitro and in vivo [21].…”

Section: Introductionmentioning

confidence: 99%

H19 gene polymorphisms and Wilms tumor risk in Chinese children: a four-center case-control study

Hua

Wang

et al. 2020

Preprint

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Background Wilms tumor is the most common pediatric renal cancer. However, genetic bases behind Wilms tumor remain largely unknown. H19 is a critical maternally imprinted gene. Previous studies indicated that nucleotide polymorphisms (SNPs) in the H19 can modify the risk of several human malignancies. Epigenetic errors at the H19 locus lead to biallele silencing in Wilms tumors. Genetic variations in the H19 may be related to Wilms tumor susceptibility. Methods We conducted a four-center study to investigate whether H19 SNPs was a predisposing factor to Wilms tumor. Three polymorphisms in the H19 (rs2839698 G>A, rs3024270 C>G, rs217727 G>A) were genotyped in 355 cases and 1070 cancer-free controls, using Taqman method. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to evaluate the strength of the associations. Results We found that all of these three polymorphisms were significantly associated with Wilms tumor risk alterations. Carriers of 1, 2 and 1-2 risk genotypes were inclined to develop Wilms tumor compared with those without risk genotype (adjusted OR=1.36, 95% CI=1.02-1.80, P=0.037; adjusted OR=1.84, 95% CI=1.27-2.67, P=0.001; adjusted OR=1.50, 95% CI=1.17-1.92, P=0.002, respectively). The stratified analysis further revealed that rs2839698 AA, rs217727 AA, and 1-2 risk genotypes could strongly increase Wilms tumor risk among male patients above 18 months of age.Conclusion Our findings indicate that genetic variations in the H19 may confer Wilms tumor risk.

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Upregulation of miR‐675‐5p induced by lncRNA H19 was associated with tumor progression and development by targeting tumor suppressor p53 in non–small cell lung cancer

Cited by 55 publications

References 39 publications

lncRNA TPTEP1 competitively sponges miR‑328‑5p to inhibit the proliferation of non‑small cell lung cancer cells

lncRNA TPTEP1 competitively sponges miR‑328‑5p to inhibit the proliferation of non‑small cell lung cancer cells

Targeted point mutations of the m6A modification in miR675 using RNA-guided base editing induce cell apoptosis

H19 gene polymorphisms and Wilms tumor risk in Chinese children: a four-center case-control study

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