LncRNA RNCR2 facilitates cell proliferation and epithelial-mesenchymal transition in melanoma through the HK2-mediated Warburg effect via targeting miR-495-3p

Duan, Baoxue; Geng, Xuerui; Wu, Yijun

doi:10.4149/neo_2021_201120n1255

Cited by 12 publications

(3 citation statements)

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“…Our study demonstrates for the first time that CREB1 participates in the regulation of MiR-495-3p is a key regulator of tumorigenesis and malignant progression. It has been reported that miR-495-3p is up-regulated in various tumour tissues, including melanoma [17]. Our findings reveal that miR-495-3p was significantly down-regulated in melanoma and that miR-495-3p overexpression inhibited melanoma cell viability.…”

Section: Discussionsupporting

confidence: 56%

CREB1 regulates KPNA2 by inhibiting mir-495-3p transcription to control melanoma progression

Geng

Qiu

Gao

et al. 2022

BMC Mol and Cell Biol

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Background Melanoma is a common type of skin cancer, and its incidence is increasing gradually. Exploring melanoma pathogenesis helps to find new treatments. Objective We aimed to explore the potential molecular mechanisms by which CREB1 regulates melanoma. Methods TransmiR and ALGGEN were used to predict targets of CREB1 in the promoter of miR-495-3p or miR-495-3p and KPNA2, and a dual-luciferase reporter assay was performed to detect binding of CREB1 to these promoters. In addition, binding of CREB1 to the miR-495-3p promoter was confirmed by a ChIP assay. qRT‒PCR was carried out to detect mRNA levels of miR-495-3p, CREB1 and KPNA2. An EdU assay was conducted to detect cell viability. Transwell assays and flow cytometry were performed to assess cell migration and invasion and apoptosis, respectively. Moreover, factors associated with overall survival were analysed by using the Cox proportional hazards model. Results Our results show miR-495-3p to be significantly decreased in melanoma. Additionally, miR-495-3p overexpression inhibited melanoma cell viability. CREB1 targeted miR-495-3p, and CREB1 overexpression enhanced melanoma cell viability by inhibiting miR-495-3p transcription. Moreover, miR-495-3p targeted KPNA2, and CREB1 regulated KPNA2 by inhibiting miR-495-3p transcription to enhance melanoma cell viability. Conclusion CREB1 regulates KPNA2 by inhibiting miR-495-3p transcription to control melanoma progression. Our results indicate the molecular mechanism by which the CREB1/miR-495-3p/KPNA2 axis regulates melanoma progression.

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Section: Discussionsupporting

confidence: 56%

CREB1 regulates KPNA2 by inhibiting mir-495-3p transcription to control melanoma progression

Geng

Qiu

Gao

et al. 2022

BMC Mol and Cell Biol

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“…Similarly, LINC00265 enhanced glycolysis and lactate release via binding with miR-216b-5p and elevating the expression of TRIM44 in colorectal cancer ( 111 ). LncRNA RNCR2 promoted glycolysis and EMT and proliferation of melanoma cells via interacting with miR-495-3p and upregulating HK2 in melanoma ( 112 ). LINC00242 combined miR-1-3p and elevated the expression of G6PD, leading to enhancement of aerobic glycolysis and oncogenesis of gastric cancer ( 113 ).…”

Section: Lncrnas Regulate Glucose Metabolism In Cancermentioning

confidence: 99%

The role of lncRNAs in regulation of DKD and diabetes-related cancer

Cheng

Xia

et al. 2022

Front. Oncol.

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Diabetes mellitus often results in several complications, such as diabetic kidney disease (DKD) and end-stage renal diseases (ESRDs). Cancer patients often have the dysregulated glucose metabolism. Abnormal glucose metabolism can enhance the tumor malignant progression. Recently, lncRNAs have been reported to regulate the key proteins and signaling pathways in DKD development and progression and in cancer patients with diabetes. In this review article, we elaborate the evidence to support the function of lncRNAs in development of DKD and diabetes-associated cancer. Moreover, we envisage that lncRNAs could be diagnosis and prognosis biomarkers for DKD and cancer patients with diabetes. Furthermore, we delineated that targeting lncRNAs might be an alternative approach for treating DKD and cancer with dysregulated glucose metabolism.

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“…Meanwhile, in a variety of tumors, lncRNAs have been shown to regulate HK-2 by targeting miRNAs, thereby affecting tumor progression [24][25][26].…”

Section: Introductionmentioning

confidence: 99%

LncRNA HCG18 promotes Prostate Cancer progression by regulating miR-512-3p/HK-2 axis

Zhu

Wang

et al. 2022

Preprint

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Long non-coding RNA (lncRNA) plays an important role in tumor progression. Numerous studies show that lncRNA is strongly associated with prostate cancer progression. Our study confirmed that lncRNA HCG18 was highly expressed in prostate cancer (PC) and correlated with tumor progression in databases and cell lines. Western blot, RNA Pull-down, dual luciferase assay and rescue assays verified the correlation among lncRNA HCG18, miR-512-3p and hexokinase-2(HK-2). In general, the results showed that lncRNA HCG18 accelerated cell proliferation, migration, and invasion of PC via up-regulating HK-2 through sponging miR-512-3p, which provided a new direction for the diagnosis and treatment of PC.

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LncRNA RNCR2 facilitates cell proliferation and epithelial-mesenchymal transition in melanoma through the HK2-mediated Warburg effect via targeting miR-495-3p

Cited by 12 publications

References 0 publications

CREB1 regulates KPNA2 by inhibiting mir-495-3p transcription to control melanoma progression

CREB1 regulates KPNA2 by inhibiting mir-495-3p transcription to control melanoma progression

The role of lncRNAs in regulation of DKD and diabetes-related cancer

LncRNA HCG18 promotes Prostate Cancer progression by regulating miR-512-3p/HK-2 axis

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