MicroRNAs as important players in regulating cancer through PTEN/PI3K/AKT signalling pathways

Selvakumar, Sushmaa Chandralekha; Preethi, K. Auxzilia; Sekar, Durairaj

doi:10.1016/j.bbcan.2023.188904

Cited by 12 publications

(4 citation statements)

References 41 publications

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“…Previous study reported that TCF12 enhances cell proliferation, migration, and invasion of hepatocellular carcinoma by activating the PI3K/AKT signaling pathway [ 34 ]. As a critical regulatory factor in the PI3K/AKT signaling pathway, PTEN regulates the Phosphoinositide 3-kinase (PI3K) and Protein Kinase B (AKT) pathway, which is involved in the cell proliferation and apoptosis of various cancers [ 35 , 36 ]. GO terms suggest that TCF12 has DNA-binding and transcription factor activity (Fig.…”

Section: Resultsmentioning

confidence: 99%

LINC00606 promotes glioblastoma progression through sponge miR-486-3p and interaction with ATP11B

Dong,

Qi,

et al. 2024

J Exp Clin Cancer Res

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Background LncRNAs regulate tumorigenesis and development in a variety of cancers. We substantiate for the first time that LINC00606 is considerably expressed in glioblastoma (GBM) patient specimens and is linked with adverse prognosis. This suggests that LINC00606 may have the potential to regulate glioma genesis and progression, and that the biological functions and molecular mechanisms of LINC00606 in GBM remain largely unknown. Methods The expression of LINC00606 and ATP11B in glioma and normal brain tissues was evaluated by qPCR, and the biological functions of the LINC00606/miR-486-3p/TCF12/ATP11B axis in GBM were verified through a series of in vitro and in vivo experiments. The molecular mechanism of LINC00606 was elucidated by immunoblotting, FISH, RNA pulldown, CHIP-qPCR, and a dual-luciferase reporter assay. Results We demonstrated that LINC00606 promotes glioma cell proliferation, clonal expansion and migration, while reducing apoptosis levels. Mechanistically, on the one hand, LINC00606 can sponge miR-486-3p; the target gene TCF12 of miR-486-3p affects the transcriptional initiation of LINC00606, PTEN and KLLN. On the other hand, it can also regulate the PI3K/AKT signaling pathway to mediate glioma cell proliferation, migration and apoptosis by binding to ATP11B protein. Conclusions Overall, the LINC00606/miR-486-3p/TCF12/ATP11B axis is involved in the regulation of GBM progression and plays a role in tumor regulation at transcriptional and post-transcriptional levels primarily through LINC00606 sponging miR-486-3p and targeted binding to ATP11B. Therefore, our research on the regulatory network LINC00606 could be a novel therapeutic strategy for the treatment of GBM. Graphical Abstract LINC00606 is highly expressed in GBM patients with carcinogenic function and correlated with poor prognosis. LINC00606 regulates glioblastoma progression by sponging miR-486-3p and interacting with ATP11B.

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Section: Resultsmentioning

confidence: 99%

LINC00606 promotes glioblastoma progression through sponge miR-486-3p and interaction with ATP11B

Dong,

Qi,

et al. 2024

J Exp Clin Cancer Res

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“…miRNAs function by inhibiting translation or causing the degradation of messenger RNA (mRNA) [ 36 ]. The PTEN /PI3K/AKT pathway plays a crucial role in cell proliferation, apoptosis, and tumor growth [ 37 ]. In a study involving rats with chronic heart failure, miR-129-5p was found to inhibit PTEN ubiquitination and enhance PTEN expression by targeting Smurf1 [ 38 ].…”

Section: Discussionmentioning

confidence: 99%

miR-129 Regulates Yak Intramuscular Preadipocyte Proliferation and Differentiation through the PI3K/AKT Pathway

Qin,

Wang,

Zhong

et al. 2024

IJMS

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miR-129 plays a crucial role in regulating various cellular processes, including adipogenesis; however, its downstream molecular mechanisms remain unclear. In this study, we demonstrated that miR-129 promotes yak adipogenesis in vitro via the PI3K/AKT pathway. Overexpression and interference of miR-129 in yak intramuscular preadipocytes (YIMAs) enhanced and inhibited cell differentiation, respectively, with corresponding changes in cell proliferation. Further investigation revealed that miR-129 enhances AKT and p-AKT activity in the AKT pathway without affecting cell apoptosis, and a specific inhibitor (LY294002) was used to confirm that miR-129 regulates YIMAs proliferation and differentiation through the PI3K/AKT pathway. Our findings suggest that miR-129 promotes yak adipogenesis by enhancing PI3K/AKT pathway activity. This study provides the foundation to precisely elucidate the molecular mechanism of miR-129 in YIMAs adipogenesis and develop advanced miRNA-based strategies to improve meat nutrition and obesity-related ailments in beef production.

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“…An increasing body of evidence supports the notion that the activated PI3K/AKT pathway is associated with the migration and invasion of malignant cells. [46][47][48] In TEAD4 activates the PI3K/AKT pathway, in turn promotes invasion and metastasis. 27 Knockdown of RPN2 gene has been shown to suppress EMT and inhibit the PI3K/AKT pathway.…”

Section: Discussionmentioning

confidence: 99%

POLR3G promotes EMT via PI3K/AKT signaling pathway in bladder cancer

Chen,

Ma,

Yang

et al. 2023

The FASEB Journal

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RNA Polymerase III Subunit G (POLR3G) promotes tumorigenesis, metastasis, cancer stemness, and chemoresistance of breast cancer and lung cancer; however, its biological function in bladder cancer (BLCA) remains unclear. Through bioinformatic analyses, we found that POLR3G expression was significantly elevated in BLCA tumor tissues and was associated with decreased survival. Multivariate Cox analysis indicated that POLR3G could serve as an independent prognostic risk factor. Our functional investigations revealed that POLR3G deficiency resulted in reduced migration and invasion of BLCA cells both in vitro and in vivo. Additionally, the expressions of EMT‐related mesenchymal markers were also downregulated in POLR3G knockdown cells. Mechanistically, we showed that POLR3G could activate the PI3K/AKT signaling pathway. Inhibition of this pathway with LY294002 reduced the enhanced migration and invasion of BLCA cells induced by POLR3G overexpression, whereas the activation of this pathway using 740Y‐P restored the abilities that were inhibited by POLR3G knockdown. Taken together, our findings suggested that POLR3G is a prognostic predictor for BLCA and promotes EMT of BLCA through activation of the PI3K/AKT signaling pathway.

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MicroRNAs as important players in regulating cancer through PTEN/PI3K/AKT signalling pathways

Cited by 12 publications

References 41 publications

LINC00606 promotes glioblastoma progression through sponge miR-486-3p and interaction with ATP11B

LINC00606 promotes glioblastoma progression through sponge miR-486-3p and interaction with ATP11B

miR-129 Regulates Yak Intramuscular Preadipocyte Proliferation and Differentiation through the PI3K/AKT Pathway

POLR3G promotes EMT via PI3K/AKT signaling pathway in bladder cancer

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