&lt;p&gt;ZFAS1 Promotes Cisplatin Resistance via Suppressing miR-421 Expression in Oral Squamous Cell Carcinoma&lt;/p&gt;

Wang, Xiaolong; Hao, Rui; Wang, Fengjuan; Wang, Fan

doi:10.2147/cmar.s248869

Cited by 15 publications

(9 citation statements)

References 33 publications

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“…NHOK, OSCC cell lines (CAL-27, Tca8113, SCC-9, and TSCCA) and DDP-resistant OSCC cell line SCC-9/DDP (all from ATCC, VA, USA) were cultured in Dulbecco’s modified Eagle’s medium containing 10% fetal bovine serum (Invitrogen, CA, USA) [ 27 ].…”

Section: Methodsmentioning

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RETRACTED ARTICLE: MIR600HG sponges miR-125a-5p to regulate glycometabolism and cisplatin resistance of oral squamous cell carcinoma cells via mediating RNF44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

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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“…Previous studies revealed that ZFAS1 acted as a sponge and negatively regulated the expression of miR-421 [ 28 , 29 ], which prompted us to hypothesize that miR-421 might be a downstream target of ZFAS1 in SH-SY5Y cells. Through using starbase website ( http://starbase.sysu.edu.cn/ ), miR-421 was predicted to bind with ZFAS1.…”

Section: Resultsmentioning

confidence: 99%

“…Zhang et al showed that lncRNA Rik-203 promoted sevoflurane-induced neurotoxicity by regulating miR-101a-3p [ 38 ]. miR-421 has been reported to facilitate neuronal apoptosis in Parkinson’s Disease [ 19 ] and epilepsy [ 20 ], and act as a downstream target of ZFAS1 in various diseases, such as oral squamous cell carcinoma [ 28 ] and epilepsy [ 29 ]. Herein, the miR-421 level was increased by bupivacaine in the time- and dose-dependent manner in SH-SY5Y cells.…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA ZFAS1 alleviates bupivacaine-induced neurotoxicity by regulating the miR-421/zinc finger protein564 (ZNF564) axis

Yuan

Guo

et al. 2021

Bioengineered

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This research aimed to explore the biological role of long non-coding RNA (lncRNA) ZFAS1 in bupivacaine-induced neurotoxicity. The levels of lncRNA ZFAS1, miR-421, and zinc finger protein 564 (ZNF564) were detected by RT-qPCR. MTT and TUNEL assays were utilized to evaluate cell viability and apoptosis, respectively. Caspase-3 activity was measured by the caspase-3 activity assay kit. The binding ability between miR-421 and ZFAS1 or ZNF564 was confirmed by Rip and dual-luciferase reporter assays. In this study, it was found that the levels of ZFAS1 and ZNF564 were gradually upregulated and miR-421 expression was downregulated with increasing concentrations of bupivacaine. Functional assays indicated that the silencing of ZFAS1 suppressed cell viability and facilitated cell apoptosis of SH-SY5Y cells, while overexpression of ZFAS1 had the opposite effects. Moreover, it was identified that miR-421 was a target of ZFAS1, and ZFAS1 regulated the bupivacaine-induced neurotoxicity via miR-421. In addition, we confirmed that ZNF564 was a downstream target of miR-421. The upregulation of miR-421 decreased the cell viability, and increased the cell apoptosis rate and caspase-3 activity, while the upregulation of ZND564 partially abolished these effects. Finally, it was demonstrated that ZFAS1 could upregulate the expression of ZNF564 by targeting miR-421. In conclusion, our results demonstrated that ZFAS1 alleviated bupivacaine-induced neurotoxicity through the miR-421/ZNF564 axis, suggesting a new strategy for the amelioration of bupivacaine-induced neurotoxicity.

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“…Exosomal lncRNA APCDD1L-AS1 conferred resistance to 5-FU via the miR-1224-5p/NSD2 axis in OSCC [ 206 ]. The expression of the lncRNA ZFAS1 attenuated miR-421 expression in OSCC, leading to the acquisition of cisplatin resistance [ 207 ].…”

Section: Extracellular Vesicles: Evsmentioning

confidence: 99%

Impact of Non-Coding RNAs on Chemotherapeutic Resistance in Oral Cancer

et al. 2022

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Drug resistance in oral cancer is one of the major problems in oral cancer therapy because therapeutic failure directly results in tumor recurrence and eventually in metastasis. Accumulating evidence has demonstrated the involvement of non-coding RNAs (ncRNAs), such as microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), in processes related to the development of drug resistance. A number of studies have shown that ncRNAs modulate gene expression at the transcriptional or translational level and regulate biological processes, such as epithelial-to-mesenchymal transition, apoptosis, DNA repair and drug efflux, which are tightly associated with drug resistance acquisition in many types of cancer. Interestingly, these ncRNAs are commonly detected in extracellular vesicles (EVs) and are known to be delivered into surrounding cells. This intercellular communication via EVs is currently considered to be important for acquired drug resistance. Here, we review the recent advances in the study of drug resistance in oral cancer by mainly focusing on the function of ncRNAs, since an increasing number of studies have suggested that ncRNAs could be therapeutic targets as well as biomarkers for cancer diagnosis.

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<p>ZFAS1 Promotes Cisplatin Resistance via Suppressing miR-421 Expression in Oral Squamous Cell Carcinoma</p>

Cited by 15 publications

References 33 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

Long non-coding RNA ZFAS1 alleviates bupivacaine-induced neurotoxicity by regulating the miR-421/zinc finger protein564 (ZNF564) axis

Impact of Non-Coding RNAs on Chemotherapeutic Resistance in Oral Cancer

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