Non‐coding RNA LOXL1-AS1 exhibits oncogenic activity in ovarian cancer via regulation of miR‐18b‐5p/VMA21 axis

Xue, Fang; Xu, Yan; Shen, C.; Qin, Zhen; Zhou, Hai

doi:10.1016/j.biopha.2019.109568

Cited by 30 publications

(20 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MiR-18b-5p had been reported to act as a tumor suppressor and downregulate downstream target mRNAs by binding with their 3′UTRs in many cancers 19 , 20 . So to explore the mechanism of miR-18b-5p’s tumor-suppressing function, three miRNA databases were used in the present study.…”

Section: Resultsmentioning

confidence: 99%

“…MiRNA microarray assay revealed that a total of 22 microRNAs were upregulated in GBC-SD cells when PVT1 was knockdown, and we selected miR-18b-5p which was related with the proliferation of GBC cells for further study. MiR-18b-5p has been reported to function as a tumor suppressor and be regulated by lncRNAs 19,20 . By analyzing the sequence of PVT1 and miR-18b-5p, no binding sites were found based on the principle of base pairing, so other mechanisms may exist by which PVT1 inhibited the expression of miR-18b-5p.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Long noncoding RNA PVT1 promoted gallbladder cancer proliferation by epigenetically suppressing miR-18b-5p via DNA methylation

et al. 2020

View full text Add to dashboard Cite

Gallbladder cancer (GBC) accounts for 85–90% malignancies of the biliary tree worldwide. Considerable evidence has demonstrated that dysregulation of lncRNAs is involved in the progression of cancer. LncRNA PVT1 has been reported to play important roles in various cancers, but its role in gallbladder cancer remains unknown. In the present study, we found that PVT1 was upregulated in GBC tissues and cells, and its upregulation was related with poor prognosis in GBC patients. PVT1 promoted GBC cells proliferation in vitro and in vivo. Mechanistically, PVT1 recruited DNMT1 via EZH2 to the miR-18b-5p DNA promoter and suppressed the transcription of miR-18b-5p through DNA methylation. Moreover, HIF1A was proved to be the downstream target gene of miR-18b-5p and PVT1 regulated GBC cells proliferation via HIF1A. In conclusion, our studies clarified the PVT1/miR-18b-5p/HIF1A regulation axis and indicated that PVT1 could be a potential therapeutic target for GBC.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA PVT1 promoted gallbladder cancer proliferation by epigenetically suppressing miR-18b-5p via DNA methylation

et al. 2020

View full text Add to dashboard Cite

show abstract

“…In addition, with so few studies to date, individual microRNA may not obviously map its function to the disease process under study. This may be seen here for the miRNAs that differed between the women with and without PCOS: miR-1260a has been reported to be associated with prostate and lung cancer and aortic aneurysms ( 37 – 39 ); similarly, miR-18b-5p has been associated with oncogenic activity ( 40 ). MiR-424-5p may stimulate an immune effect through the mTOR pathway ( 41 ) and it has been shown that mTOR signaling was responsible for excessive follicle activation and growth in an animal model of PCOS ( 42 ).…”

Section: Discussionmentioning

confidence: 72%

Increased MicroRNA Levels in Women With Polycystic Ovarian Syndrome but Without Insulin Resistance: A Pilot Prospective Study

et al. 2020

View full text Add to dashboard Cite

Background: Small noncoding microRNA (miRNA) have regulatory functions in polycystic ovary syndrome (PCOS) that differ to those in women without PCOS. However, little is known about miRNA expression in women with PCOS who are not insulin resistant (IR). Methods: Circulating miRNAs were measured using quantitative polymerase chain reaction (qPCR) in 24 non-obese BMI and age matched women with PCOS and 24 control women. A miRNA data set was used to determine miRNA levels. Results: Women with PCOS showed a higher free androgen index (FAI) and anti-mullerian hormone (AMH) but IR did not differ. Four miRNAs (miR-1260a, miR-18b-5p, miR-424-5p, and miR let-7b-3p) differed between control and PCOS women that passed the false discovery rate (FDR) out of a total of 177 circulating miRNAs that were detected. MiRNA let-7b-3p correlated with AMH in PCOS (p < 0.05). When the groups were combined, miR-1260a correlated with FAI and let-7b-3p correlated with body mass index (BMI) (p < 0.05). There was no correlation to androgen levels. Ingenuity pathway analysis showed that nine of the top 10 miRNAs reported were associated with inflammatory pathways. Conclusion: When IR did not differ between PCOS and control women, only four miRNA differed significantly suggesting that IR may be a driver for many of the miRNA changes reported. Let-7b-3p was related to AMH in PCOS, and to BMI as a group, whilst miR-1260a correlated with FAI. Androgen levels, however, had no effect upon circulating miRNA profiles. The expressed miRNAs were associated with the inflammatory pathway involving TNF and IL6.

show abstract

“…microRNA-376b (miR-376b) might act as a tumor promotor in breast cancer [26] and as a tumor suppressor in clinical nonfunctioning pituitary adenomas (CNFPAs) [27] by targeting Hoxd10. microRNA-18b (miR-18b) might act as a tumor promotor in Ovarian cancer (OC) [28], hepatoma [29] and Colorectal Cancer [30] and as a tumor suppressor in Ovarian cancer (OC) [31] and breast cancer [32] by targeting PTEN, NUSAP1,CDKN2B, VMA21, LOXL1-AS1 or MDM2. In the present study, Three hub miRNAs (miR-539, miR-376b and miR-18b) were identi ed to be involved into imatinib-resistant.…”

Section: Discussionmentioning

confidence: 99%

APOBEC3B and SPAG5, the Target Genes of miR-539, Involved into Imatinib-Resistant of Gastrointestinal Stromal Tumors

Zhang¹,

Liu²,

Li³

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Although imatinib can effectively treat gastrointestinal stromal tumor (GIST), some patients are still resistant to it or cannot tolerate the adverse reactions of the drug. This study aimed to investigate potential miRNAs, mRNA and tumor-infiltrating lymphocytes (TILs) associated with the prognosis of imatinib-resistant GIST.Methods: mRNA, miRNA sequencing data and patient clinic traits of primary (imatinib-naive) and imatinib-resistant GIST were obtained from GEO (Gene Expression Omnibus) database. A systems biology approach combining Weighted co-expression network analysis (WGCNA) and differential expression analysis were utilized to detect the imatinib-resistant-related miRNA and gene modules and construct a miRNA-gene network. Tumor-infiltrating immune cells were analyzed by Estimating the Proportion of Immune and Cancer cells (EPIC) and Tumor-Immune System Interactions (TISIDB). miR-539 was measured by qRT-PCR. SPAG5 and APOBEC3B was measured by qRT-PCR and WB. Transforming growth factor (TGF)-β and interleukin (IL)-10 were assessed with enzyme-linked immunosorbent assay (ELISA). The proportions of CD4+ T cells, CD8+ T cells , NK cells and B cells in tumor-infiltrating lymphocyteswere analyzed via flow cytometry (FCM).Results: Two gene modules (brown and yellow) and one miRNA module were associated with the imatinib-resistant. Two hub genes (APOBEC3B and SPAG5) were associated with the imatinib-resistant. Three hub miRNAs were identified to be related to imatinib-resistant (miR-539, miR-376b and miR-18b). G1/S transition of mitotic cell cycle, G2/M transition of mitotic cell cycle, and cell proliferation were common pathways of the gene modules and miRNA module. apolipoprotein B mRNA editing catalytic polypeptide-like 3B (APOBEC3B) and Sperm-associated antigen 5 (SPAG5), which were both target genes of miR-539 was located at the core of miRNA–gene network. APOBEC3B (rho=0.509, p < 2.2e-16) and SPAG5 (rho=0.468, p < 2.2e-16) was positive correlated with the infiltration levels of activated CD4+ T cells. he proportions of CD4+ T cells, and the mRNA and protein relative expression of APOBEC3B and SPAG5 in imatinib-resistant tumor samples significantly increased as compared with tumor samples in imatinib-naive group. Imatinib-resistant tumor samples exhibited significantly downregulation of miR-539 and TGF-β1. Over-expression of miR-539 sensitized imatinib resistant GIST48 cells and increased the secretion of TGF-β1 by inhibiting APOBEC3B and SPAG5.Conclusion: APOBEC3B and SPAG5, the target genes of miR-539 may play as key factor for imatinib-resistant GIST by increasing the proportion of tumor-infiltrated activated CD4+ T cells via TGF-β1. These findings help to advance the understanding of imatinib-resistant GIST and provide potential therapeutic targets.

show abstract

Non‐coding RNA LOXL1-AS1 exhibits oncogenic activity in ovarian cancer via regulation of miR‐18b‐5p/VMA21 axis

Cited by 30 publications

References 19 publications

Long noncoding RNA PVT1 promoted gallbladder cancer proliferation by epigenetically suppressing miR-18b-5p via DNA methylation

Long noncoding RNA PVT1 promoted gallbladder cancer proliferation by epigenetically suppressing miR-18b-5p via DNA methylation

Increased MicroRNA Levels in Women With Polycystic Ovarian Syndrome but Without Insulin Resistance: A Pilot Prospective Study

APOBEC3B and SPAG5, the Target Genes of miR-539, Involved into Imatinib-Resistant of Gastrointestinal Stromal Tumors

Contact Info

Product

Resources

About