Down‐regulated lncRNA SLC25A5‐AS1 facilitates cell growth and inhibits apoptosis via miR‐19a‐3p/PTEN/PI3K/AKT signalling pathway in gastric cancer

Li, Xiwen; Yan, Xin; Wang, Feng; Yang, Qian; Luo, Xi; Kong, Jun Suk; Ju, Shaoqing

doi:10.1111/jcmm.14200

Cited by 61 publications

(47 citation statements)

References 44 publications

(84 reference statements)

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“…17 Li et al found that lncRNA SLC25A5-AS1 reduced GC cells growth by regulating miR-19a-3p/PTEN/PI3K/AKT axis. 18 However, the roles and underlying mechanisms of lncRNAs in GC remain unclear.…”

Section: Discussionmentioning

confidence: 99%

<p>Long non-coding RNA LINC00665 gastric cancer tumorigenesis by regulation miR-149-3p/RNF2 axis</p>

Qi¹,

Xiao²,

Yun-xi³

2019

OTT

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Background: Recently, LINC00665 has been reported to be a pivotal regulator in kinds of malignancy, such as lung cancer and liver cancer. However, the functions and underlying mechanisms of LINC00665 in gastric cancer (GC) remain unclear. Materials and methods: We recruited 49 paired GC tissue to explore LINC00665 expression by qRT-PCR. In vitro function assays were used to explore the roles of LINC00665 in GC progression. Moreover, the interaction among LINC00665, miR-149-3p and RNF2 was explored by bioinformatics analysis and luciferase reporter assay. Results: In the present study, we found that LINC00665 expression was significantly elevated in GC tissues and cell lines. High LINC00665 expression was associated with TNM stage, histological grade, and poor prognosis of GC patients. Function assays showed that LINC00665 suppression significantly reduced GC cells viability and invasion ability in vitro. Mechanistic analysis showed that LINC00665 might serve as a ceRNA for miR-149-3p to regulate the expression of RNF2. Conclusion: Our current study revealed the LINC00665/miR-149-3p/RNF2 axis was involved in GC progression, providing novel insights into the treatment for GC.

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Section: Discussionmentioning

confidence: 99%

<p>Long non-coding RNA LINC00665 gastric cancer tumorigenesis by regulation miR-149-3p/RNF2 axis</p>

Qi¹,

Xiao²,

Yun-xi³

2019

OTT

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“…PI3K/AKT/NF-κB and PI3K/AKT/ mTOR are the two main mutated pathways involved in apoptosis and tumorigenesis, and these pathways are related to MDR. The dysregulation of the major components of these two signaling pathways that leads to the activation of certain targets to promote MDR in many types of cancers is discussed below 58 .…”

Section: Aberrant Activation Of the Pi3k/akt/nf-κb And Pi3k/akt/mtor mentioning

confidence: 99%

PI3K/AKT pathway as a key link modulates the multidrug resistance of cancers

et al. 2020

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Multidrug resistance (MDR) is the dominant challenge in the failure of chemotherapy in cancers. Phosphatidylinositol 3-kinase (PI3K) is a lipid kinase that spreads intracellular signal cascades and regulates a variety of cellular processes. PI3Ks are considered significant causes of chemoresistance in cancer therapy. Protein kinase B (AKT) is also a significant downstream effecter of PI3K signaling, and it modulates several pathways, including inhibition of apoptosis, stimulation of cell growth, and modulation of cellular metabolism. This review highlights the aberrant activation of PI3K/AKT as a key link that modulates MDR. We summarize the regulation of numerous major targets correlated with the PI3K/AKT pathway, which is further related to MDR, including the expression of apoptosis-related protein, ABC transport and glycogen synthase kinase-3 beta (GSK-3β), synergism with nuclear factor kappa beta (NF-κB) and mammalian target of rapamycin (mTOR), and the regulation of glycolysis.

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“…A series of lncRNAs have been underscored. LncRNA SLC25A5-AS1 restores the expression and function of PTEN via acting as a miR-19a-3p in suppressing malignant phenotypes in gastric cancer [18]. LncRNA SNHG20 facilitates the downstream target ZEB2 and RUNX2 via sponging miR-154 in promoting non-small cell lung cancer progression [19].…”

Section: Introductionmentioning

confidence: 99%

FOXC1-induced LINC01123 acts as a mediator in triple negative breast cancer

et al. 2020

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Background: MicroRNAs (miRNAs) representing a subclass of non-coding RNAs are dynamically expressed and participate in multiple pathological responses, whereas, the expression pattern or function of miRNAs has not been fully addressed in triple-negative breast cancer (TNBC). Currently we concentrate on dissecting the probable role of microRNA-663a (miR-663a) in TNBC cellular processes. Methods: qRT-PCR detected the expression of miR-663a in TNBC cells. Besides, we monitored the effects of miR-663a on TNBC proliferation and apoptosis. On the basis of bioinformatics assistance and mechanical validation, we identified the miRNA-sponging role of LINC01123 and downstream target of miR-663a in TNBC was assessed and verified. The transcription activation of was explored via ChIP and luciferase reporter assays. Results: In comparison to MCF-10A, we certified the downregulation of miR-663a in TNBC cell lines. Augmentation of miR-663a was anti-proliferation and pro-apoptosis in TNBC cell lines. LINC01123 protected CMIP against miR-663a suppression through acting as a sponge of miR-663a in TNBC. LINC01123 was transcriptionally induced by FOXC1. Rescue experiment proved that miR-663a suppression or CMIP (c-Maf inducing protein) enhancement could countervail LINC01123 depletion-mediated effects on TNBC cellular processes. Conclusion: LINC01123, activated by FOXC1, regulated TNBC growth through miR-663a/CMIP signaling, which unveiled a new functional pathway of FOXC1-induced LINC01123/miR-663a/CMIP in TNBC.

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Down‐regulated lncRNA SLC25A5‐AS1 facilitates cell growth and inhibits apoptosis via miR‐19a‐3p/PTEN/PI3K/AKT signalling pathway in gastric cancer

Cited by 61 publications

References 44 publications

<p>Long non-coding RNA LINC00665 gastric cancer tumorigenesis by regulation miR-149-3p/RNF2 axis</p>

<p>Long non-coding RNA LINC00665 gastric cancer tumorigenesis by regulation miR-149-3p/RNF2 axis</p>

PI3K/AKT pathway as a key link modulates the multidrug resistance of cancers

FOXC1-induced LINC01123 acts as a mediator in triple negative breast cancer

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