lncRNA CASC11 promotes cancer cell proliferation in bladder cancer through miRNA‐150

Luo, Huarong; Xu, Chengdang; Le, Wei; Ge, Bujun; Wang, Tianru

doi:10.1002/jcb.28622

Cited by 107 publications

(76 citation statements)

References 24 publications

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“…The transcription factor c-Myc represses miR-129-5p expression in hepatocellular carcinoma ( Han et al, 2016 ). Overexpression of lncRNA CASC11 promotes bladder cancer cell proliferation via inhibition of miR-150 expression ( Luo et al, 2019 ). The mechanisms by which miR-16-1-3p is repressed in breast cancer require to be investigated.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-16-1-3p Represses Breast Tumor Growth and Metastasis by Inhibiting PGK1-Mediated Warburg Effect

Liang²,

Zhang³

et al. 2020

Front. Cell Dev. Biol.

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The Warburg effect (aerobic glycolysis) is a hallmark of cancer and is becoming a promising target for diagnosis and therapy. Phosphoglycerate kinase 1 (PGK1) is the first adenosine triphosphate (ATP)-generating glycolytic enzyme in the aerobic glycolysis pathway and plays an important role in cancer development and progression. However, how microRNAs (miRNAs) regulate PGK1-mediated aerobic glycolysis remains unknown. Here, we show that miR-16-1-3p inhibits PGK1 expression by directly targeting its 3′-untranslated region. Through inhibition of PGK1, miR-16-1-3p suppressed aerobic glycolysis by decreasing glucose uptake, lactate and ATP production, and extracellular acidification rate, and increasing oxygen consumption rate in breast cancer cells. Aerobic glycolysis regulated by the miR-16-1-3p/PGK1 axis is critical for modulating breast cancer cell proliferation, migration, invasion and metastasis in vitro and in vivo. In breast cancer patients, miR-16-1-3p expression is negatively correlated with PGK1 expression and breast cancer lung metastasis. Our findings provide clues regarding the role of miR-16-1-3p as a tumor suppressor in breast cancer through PGK1 suppression. Targeting PGK1 through miR-16-1-3p could be a promising strategy for breast cancer therapy.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-16-1-3p Represses Breast Tumor Growth and Metastasis by Inhibiting PGK1-Mediated Warburg Effect

Liang²,

Zhang³

et al. 2020

Front. Cell Dev. Biol.

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“…The statistical assay showed that the expression of LINC00662 in BC tissues was negatively correlated with the 5-year survival rate of the patients. LncRNA can absorb specific miRNA by sponge effect or competitively bind miRNA to regulate the binding of endogenous miRNA to its target gene 26 . In this study, we predicted and validated the possible interact target of LINC00662.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA LINC00662 facilitates bladder cancer progression through modulating miR-195-5p/VEGFA/Ras/Raf/MEK/ERK signaling pathway

Wang

Niu

Jiang

et al. 2020

Preprint

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Background: Bladder cancer (BC) is one of the most common malignant tumors in the urinary system. Long non-coding RNA (lncRNA) plays an important role in BC. Methods: LINC00662 expression was identified by quantitative real-time polymerase chain reaction (qPCR) and in situ hybridization (ISH). The effect of LINC00662 on cell proliferation, apoptosis, migration and invasion was measured by CCK8 assay, colony formation assay, transwell assay, and western blot. Dual-luciferase reporter gene assay, RNA pull-down and RIP assay confirm the interaction between LINC00662 and miR-195-5p/VEGFA. The in vivo effect of LINC00662 on BC was investigated using a mouse tumorigenicity model. Results: LINC00662 was overexpressed in BC tissues and cell lines, and negatively correlated with the survival of BC patients. Overexpression of LINC00662 promoted proliferation, migration and invasion and inhibited apoptosis of BC cells, and LINC00662 knockdown abrogated this effect. Silencing LINC00662 inhibited BC growth in a subcutaneous BC tumor mouse model. LINC00662 acted as an oncogene through regulating miR-195-5p/VEGFA axes. Decreased VEGFA expression caused by LINC00662 knockdown inhibited the phosphorylation of Raf-1, MEK1/2, and ERK1/2, while this regulation effect was abrogated by miR-195-5p inhibitor. Conclusion: LINC00662 regulated the proliferation, apoptosis, migration, and invasion of BC cells probably via miR-195-5p-mediated VEGFA/Ras/Raf/MEK/ERK signaling pathway.

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“…The contribution of lncRNAs to the growth, proliferation and survival of different types of cancer has been studied ( 36 , 46 , 79 – 83 ) Several studies have emphasized the potential of lncRNAs in promoting metastasis in breast cancer cell lines and tissues ( 84 , 85 ). Dysregulation of lncRNA inhibiting proliferation and metastasis ( NLIPMT ) has been reported to enhance growth and metastasis in breast cancer tissue.…”

Section: Role Of Lncrna In Breast Cancermentioning

confidence: 99%

“…Long non-coding RNAs (lncRNAs) are RNA molecules in the range of 200–2,000 bp ( 32 ). lncRNAs have been found to play a crucial role in the development of various cancer types, including breast ( 33 ), thyroid ( 34 ), renal ( 35 ), colorectal ( 36 ), prostate ( 37 ) and ovarian cancer ( 38 ), and have been reported to interact with various molecules during transcription, chromosome remodeling, cellular trafficking and translation ( 39 ). In addition, lncRNAs serve regulatory roles during transcription, mRNA processing, maturation of mRNAs, modification of histone complexes and DNA methyltransferase modifications that occur during epigenetic regulation ( Fig.…”

Section: Introductionmentioning

confidence: 99%

Long non‑coding RNA regulation of TRAIL in breast cancer: A tangle of non‑coding threads (Review)

et al. 2020

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Breast cancer is a complex disease posing a serious threat to the female population worldwide. A complex molecular landscape and tumor heterogeneity render breast cancer cells resistant to drugs and able to promote metastasis and invasiveness. Despite the recent advancements in diagnostics and drug discovery, finding an effective cure for breast cancer is still a major challenge. Positive and negative regulation of apoptosis has been a subject of extensive study over the years. Numerous studies have shed light on the mechanisms that impede the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) signaling cascade. Long non-coding RNAs (lncRNAs) have been implicated in the orchestration, development, proliferation, differentiation and metastasis of breast cancer. However, the roles of lncRNAs in fine-tuning apoptosis regulating machinery in breast cancer remain to be elucidated. The present review illuminates the roles of these molecules in the regulation of breast cancer and the interplay between lncRNA and TRAIL in breast cancer. The present review also attempts to reveal their role in the regulation of apoptosis in breast cancer appears a promising approach for the development of new diagnostic and therapeutic regimens.

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lncRNA CASC11 promotes cancer cell proliferation in bladder cancer through miRNA‐150

Cited by 107 publications

References 24 publications

MicroRNA-16-1-3p Represses Breast Tumor Growth and Metastasis by Inhibiting PGK1-Mediated Warburg Effect

MicroRNA-16-1-3p Represses Breast Tumor Growth and Metastasis by Inhibiting PGK1-Mediated Warburg Effect

Long non-coding RNA LINC00662 facilitates bladder cancer progression through modulating miR-195-5p/VEGFA/Ras/Raf/MEK/ERK signaling pathway

Long non‑coding RNA regulation of TRAIL in breast cancer: A tangle of non‑coding threads (Review)

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