Long non‑coding RNA OIP5‑AS1 contributes to cisplatin resistance of oral squamous cell carcinoma through the miR‑27b‑3p/TRIM14 axis

Zhang, Xiao; Li, Jiayi; Jin, Qingsong; Liu, Dongxiu

doi:10.3892/etm.2021.9839

Cited by 16 publications

(7 citation statements)

References 13 publications

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“…Therefore, it is of importance to investigate diagnostic strategies and find therapeutic targets to improve the treatment of OSCC. Cisplatin (DDP) is an effective first-line chemotherapy drug for OSCC treatment, while its therapeutic effect often fails as a result of the drug resistance [ 3 ]. Tumor cells can take up more glucose, and glucose undergo aerobic glycolytic synthesis to generate more intermediate substances and eventually to generate lactic acid.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: MIR600HG sponges miR-125a-5p to regulate glycometabolism and cisplatin resistance of oral squamous cell carcinoma cells via mediating RNF44

et al. 2022

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There is increasing evidence that dysregulated long non-coding RNA (lncRNA) is implicated in tumorigenesis and progression. We aim to explore the role of lncRNA MIR600HG in glycometabolism and cisplatin (DDP) resistance of oral squamous cell carcinoma (OSCC) cells via regulating microRNA-125a-5p (miR-125a-5p) and RING finger 44 (RNF44). Expression of MIR600HG, miR-125a-5p, and RNF44 in OSCC clinical samples, cell lines, and DDP-resistant OSCC cells (SCC-9/DDP) was determined. In SCC-9 cells, proliferation, IC50 value of DDP, migration, invasion, and apoptosis were detected; in SCC-9/DDP cells, proliferation, IC50 value of DDP, apoptosis, glucose consumption, and production of lactic acid and ATP were evaluated. The interaction of MR600HG, miR-125a-5p, and RNF44 was verified. MIR600HG and RNF44 were upregulated while miR-125a-5p was downregulated in OSCC tissues and cell lines, and also in SCC-9/DDP cells. In SCC-9 cells, MIR600HG overexpression improved cell growth, metastasis, and inhibited cell susceptibility to DDP; in SCC-9/DDP cells, silencing of MIR600HG promoted apoptosis, improved DDP sensitivity, and inhibited cell glycolysis. Downregulation of miR-125a-5p showed the opposite effect to downregulation of MIR600HG. MIR600HG bound to miR-125a-5p and miR-125a-5p targeted RNF44. Downregulation of miR-125a-5p reversed the improvement of DDP sensitivity and the inhibition of cell glycolysis by downregulated MIR600HG on SCC-9/DDP cells. Downregulating RNF44 reversed the promotion of DDP resistance and cell glycolysis of SCC-9/DDP cells mediated by downregulation of miR-125a-5p. Collectively, our study addresses that MIR600HG downregulation elevates miR-125a-5p and reduces RNF44 expression, thereby improving DDP sensitivity and inhibiting glycolysis in DDP-resistant OSCC cells.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: MIR600HG sponges miR-125a-5p to regulate glycometabolism and cisplatin resistance of oral squamous cell carcinoma cells via mediating RNF44

et al. 2022

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“…reported that OIP5-AS1 increased cisplatin resistance via binding with miR-340-5p and upregulating LPAATβ and PI3K/AKT/mTOR pathway in osteosarcoma ( 44 ). Similarly, OIP5-AS1 promoted cisplatin resistance via regulating miR-27b-3p/TRIM14 axis in oral squamous cell carcinoma ( 45 ). Liang et al.…”

Section: Discussionmentioning

confidence: 99%

LncRNA OIP5-AS1 Knockdown Targets miR-183-5p/GLUL Axis and Inhibits Cell Proliferation, Migration and Metastasis in Nasopharyngeal Carcinoma

Tang

Zen

et al. 2022

Front. Oncol.

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Nasopharyngeal carcinoma (NPC) is often associated with the infection of Epstein-Barr virus in nasopharynx and is mainly happened in South China and Southeast Asia. Recently, noncoding RNAs have been reported to regulate NPC carcinogenesis. LncRNA OIP5-AS1 participates in tumorigenesis and progression; however, the inherent mechanism of OIP5-AS1-mediated progression of NPC is unclear. In the current study, we aimed to explore the role of OIP5-AS1 in NPC progression. We measured the cell viability, apoptosis, migration, and invasion in NPC cells after OIP5-AS1 modulation. Moreover, we determined whether OIP5-AS1 exerts its oncogenic functions via sponging miR-183-5p in NPC. Furthermore, we determined whether glutamate ammonia ligase (GLUL) was a downstream target of miR-183-5p. We found that OIP5-AS1 downregulation inhibited the viability, migration and invasion of NPC via targeting miR-183-5p. We also identified that GLUL might be a potential downstream target of miR-183-5p in NPC cells. Mechanistically, OIP5-AS1 promotes cell motility via regulating miR-183-5p and GLUL in NPC cells. We concluded that OIP5-AS1 performed its biological functions via targeting miR-183-5p and GLUL in NPC cells.

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“…RT-qPCR reactions were performed in a total volume of 10 µl, including 2.5 µl cDNA, 5 µl SYBR Premix, 0.25 µl each of paired primers, and 2 µl ddH 2 O [22]. LINC01128 was normalized by glyceraldehyde phosphate dehydrogenase (GAPDH), and miR-27b-3p was normalized by U6 [32]. Expression levels of LINC01128 and miR-27b-3p were calculated by 2 -ΔΔCt method.…”

Section: Rt-qpcr Assaymentioning

confidence: 99%

Long non-coding RNA LINC01128 affects proliferation, migration, and invasion of glioma cells by regulating miR-27b-3p

Zhang¹,

Shao²,

Li³

et al. 2022

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Introduction: Glioma is a collective term for tumors derived from glial cells and neuronal cells in the nervous system, and is the most common malignant tumor in the brain. Nowadays, the problem of poor treatment effect and high recurrence rate of patients remains to be solved. Material and methods: In this study, the expression levels of LINC01128 in glioma tissues, cells, and normal control group were determined by real-time quantitative PCR (RT-qPCR). Kaplan-Meier curve was used to evaluate the prognosis and survival. Multivariate Cox analysis was chosen to estimate the prognostic risk factors of glioma. Cell counting kit-8 (CCK-8) and Transwell methods were used to detect the effect of silencing LINC01128 on the proliferation, migration, and invasion of glioma cells, and the targeting effect of LINC01128 on miR-27b-3p was determined based on bio-informatics analysis and luciferase activity detection.Results: LINC01128 was up-regulated in glioma tissues and cells. The possibility of LINC01128 as a prognostic factor of glioma was obtained through Kaplan-Meier's clinical data analysis and multivariate Cox analysis. Silencing LINC01128 targeting miR-27b-3p inhibited the proliferation, migration, and invasion activity of glioma cells. Moreover, there was a negative correlation between LINC01128 and miR-27b-3p. Conclusions: Silencing LINC01128 inhibited the proliferation, migration, and invasion levels of glioma cells by targeting miR-27b-3p, thereby affecting the progression of gliomas.

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Long non‑coding RNA OIP5‑AS1 contributes to cisplatin resistance of oral squamous cell carcinoma through the miR‑27b‑3p/TRIM14 axis

Cited by 16 publications

References 13 publications

RETRACTED ARTICLE: MIR600HG sponges miR-125a-5p to regulate glycometabolism and cisplatin resistance of oral squamous cell carcinoma cells via mediating RNF44

RETRACTED ARTICLE: MIR600HG sponges miR-125a-5p to regulate glycometabolism and cisplatin resistance of oral squamous cell carcinoma cells via mediating RNF44

LncRNA OIP5-AS1 Knockdown Targets miR-183-5p/GLUL Axis and Inhibits Cell Proliferation, Migration and Metastasis in Nasopharyngeal Carcinoma

Long non-coding RNA LINC01128 affects proliferation, migration, and invasion of glioma cells by regulating miR-27b-3p

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