&lt;p&gt;Silencing of Long Non-Coding RNA-HCG18 Inhibits the Tumorigenesis of Gastric Cancer Through Blocking PI3K/Akt Pathway&lt;/p&gt;

Ma, Feng-Zhen; An, Kexiang; Li, Yuqin

doi:10.2147/ott.s240965

Cited by 22 publications

(21 citation statements)

References 30 publications

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“…To confirm whether circ‐PRMT5 exerts its effects in breast cancer via the miR‐509‐3p/TCF7L2 axis and the PI3K/AKT pathway, we performed the subsequent rescue assays. 740 Y‐P, a well‐known activator of the PI3K/AKT pathway, was used at a concentration of 20 μg/mL 20,21 . As shown in Figure 6A,B, breast cancer cell viability and proliferation capacity were inhibited by down‐regulated circ‐PRMT5 but restored after overexpressing pcDNA3.1/TCF7L2.…”

Section: Resultsmentioning

confidence: 99%

Circ‐PRMT5 promotes breast cancer by the miR‐509‐3p/TCF7L2 axis activating the PI3K/AKT pathway

Jia

Zhang

et al. 2020

The Journal of Gene Medicine

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BackgroundBreast cancer is the most prevalent malignancy occurring in females. In recent years, emerging evidence has suggested that circular RNAs are involved in the development of multiple cancers. Circ‐PRMT5 has recently attracted attention as a tumor‐promoting circular RNA. In the present study, we focused on exploring the biological effects of circ‐PRMT5 in breast cancer.MethodsA quantitative real‐time polymerase chain reaction was used to determine the expression of circ‐PRMT5 in breast cancer. In vitro experiments, including cell‐counting kit‐8, 5‐ethynyl‐2'‐deoxyuridine, flow cytometry and tube formation assays, were performed to test the effects of circ‐PRMT5 on the cellular progression of breast cancer. Bioinformatic analysis, luciferase reporter, radioimmunoprecipitation and RNA‐pull down assays were performed to predict the potential microRNAs interacting with circ‐PRMT5 and mRNAs that can be targeted by miR‐509‐3p.ResultsCirc‐PRMT5 is up‐regulated in breast cancer tissues and cells. Importantly, an elevation of circ‐PRMT5 indicates a poor prognosis in patients with breast cancer. Functionally, knockdown of circ‐PRMT5 suppresses cell proliferation and angiogenesis and increases cell apoptosis in breast cancer. Mechanistically, we identified that circ‐PRMT5 up‐regulates TCF7L2 expression by acting as a miR‐509‐3p sponge. The negative expression correlation between miR‐509‐3p and circ‐PRMT5 or TCF7L2 in clinical tissues was further demonstrated. Rescue assays showed that TCF7L2 overexpression reverses the antitumoral effects of circ‐PRMT5 knockdown on breast cancer cell processes. Additionally, we demonstrated that circ‐PRMT5 activates the phosphoinositide 3‐kinase (PI3K)/AKT pathway by up‐regulation of TCF7L2.ConclusionsOverall, our data indicate that the circ‐PRMT5/miR‐509‐3p/TCF7L2 axis can aggravate the malignant character of breast cancer cells by the regulation of the PI3K/AKT pathway.

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Section: Resultsmentioning

confidence: 99%

Circ‐PRMT5 promotes breast cancer by the miR‐509‐3p/TCF7L2 axis activating the PI3K/AKT pathway

Jia

Zhang

et al. 2020

The Journal of Gene Medicine

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“…So far, a number of evidence show that lncRNAs are involved in tumor progression and cisplatin resistance of gastric cancer via various mechanisms. [25][26][27][28] NUTM2A-AS1 has not been studied in cancer, including gastric cancer. Our group, for the first time, prove that NUTM2A-AS1 accelerates tumor invasion, angiogenesis, and cisplatin resistance at cellular and animal level.…”

Section: Discussionmentioning

confidence: 99%

“…So far, a number of evidence show that lncRNAs are involved in tumor progression and cisplatin resistance of gastric cancer via various mechanisms 25‐28 . NUTM2A‐AS1 has not been studied in cancer, including gastric cancer.…”

Section: Discussionmentioning

confidence: 99%

LncRNA NUTM2A‐AS1 positively modulates TET1 and HIF‐1A to enhance gastric cancer tumorigenesis and drug resistance by sponging miR‐376a

Wang

et al. 2020

Cancer Medicine

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“…23 A recent GC study demonstrates that HCG18 regulates the tumorigenesis via PI3K/ Akt pathway. 24 Thus, it can be seen that HCG18 exerts an important function in regulating the biological characteristics of tumors, but its function in human tumors is controversial. Our research is consistent with the previous report, 24 which reveals that HCG18 expression in GC tissues was remarkably higher than normal paracancerous tissues, and highly expressed HCG18 was strongly linked to a larger tumor size, lymph node IVS, and distal MTS.…”

Section: Discussionmentioning

confidence: 99%

“…24 Thus, it can be seen that HCG18 exerts an important function in regulating the biological characteristics of tumors, but its function in human tumors is controversial. Our research is consistent with the previous report, 24 which reveals that HCG18 expression in GC tissues was remarkably higher than normal paracancerous tissues, and highly expressed HCG18 was strongly linked to a larger tumor size, lymph node IVS, and distal MTS. Additionally, high HCG18 expression was linked to GC adverse prognosis and could be used as a prognosis predictive factor.…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA HCG18 up‐regulates the expression of WIPF1 and YAP/TAZ by inhibiting miR‐141‐3p in gastric cancer

et al. 2020

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Background Accumulating works show that lncRNAs play critical roles in the development of gastric cancer (GC). LncRNA HLA complex group 18 (HCG18) was implicated in the progression of bladder cancer and glioma, but its role in GC is unknown. Methods RT‐PCR was used to detect HCG18 and miR‐141‐3p expression in GC specimen. GC cell lines (AGS and MKN‐28) were exploited as cell model. The biological effect of HCG18 on cancer cells was probed by CCK‐8, colony formation, flow cytometry, Transwell and wound‐healing experiments in vitro, and subcutaneous xenotransplanted tumor model and tail vein injection model in vivo. Interaction between HCG18 and miR‐141‐3p was determined by bioinformatics analysis, RT‐PCR, and luciferase reporter experiments. Downstream gene expression of miR‐141‐3p, including Wiskott–Aldrich syndrome protein interacting protein family member 1 (WIPF1), Yes associated protein 1 (YAP), and tafazzin (TAZ) were detected using Western blot. Results HCG18 was markedly up‐regulated in GC specimens, while miR‐141‐3p was markedly down‐regulated. Down‐regulation of HCG18 inhibited viability, migration, and invasion of GC cells, while miR‐141‐3p transfection led to opposite effect. HCG18 could down‐regulate miR‐141‐3p through adsorbing it, and a negative association between HCG18 and miR‐141‐3p was found in GC specimens. HCG18 promoted WIPF1, YAP and TAZ expression, nonetheless, such influence was reversed by co‐transfecting with miR‐141‐3p. Conclusion HCG18 was aberrantly up‐regulated in GC tissues, and it indirectly regulated the activity of Hippo signaling through counteracting miR‐141‐3p expression.

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<p>Silencing of Long Non-Coding RNA-HCG18 Inhibits the Tumorigenesis of Gastric Cancer Through Blocking PI3K/Akt Pathway</p>

Cited by 22 publications

References 30 publications

Circ‐PRMT5 promotes breast cancer by the miR‐509‐3p/TCF7L2 axis activating the PI3K/AKT pathway

Circ‐PRMT5 promotes breast cancer by the miR‐509‐3p/TCF7L2 axis activating the PI3K/AKT pathway

LncRNA NUTM2A‐AS1 positively modulates TET1 and HIF‐1A to enhance gastric cancer tumorigenesis and drug resistance by sponging miR‐376a

Long noncoding RNA HCG18 up‐regulates the expression of WIPF1 and YAP/TAZ by inhibiting miR‐141‐3p in gastric cancer

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