scholarly journals Recent advances in the contribution of noncoding RNAs to cisplatin resistance in cervical cancer

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e9234
Author(s):  
Xin Wen ◽  
Shui Liu ◽  
Jiyao Sheng ◽  
Manhua Cui
Keyword(s):  
Cervical Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Treatment Option ◽  
Disease Burden ◽  
Cisplatin Resistance ◽  
Noncoding Rnas ◽  
Mechanisms Of Action ◽  
Female Population ◽  
Cellular Processes

Cervical cancer (CC) remains a major disease burden on the female population worldwide. Chemotherapy with cisplatin (cis-diamminedichloroplatinum (II); CDDP) and related drugs are the main treatment option for CC; however, their efficacy is limited by the development of drug resistance. Noncoding RNAs (ncRNAs) have been found to play critical roles in numerous physiological and pathological cellular processes, including drug resistance of cancer cells. In this review, we describe some of the ncRNAs, including miRNAs, lncRNAs and circRNAs, that are involved in the sensitivity/resistance of CC to CDDP-based chemotherapy and discuss their mechanisms of action. We also describe some ncRNAs that could be therapeutic targets to improve the sensitivity of CC to CDDP-based chemotherapy.

scholarly journals Sema4C mediates EMT inducing chemotherapeutic resistance of miR-31-3p in cervical cancer cells

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Li Jing ◽  
Wang Bo ◽  
Feng Yourong ◽  
Wang Tian ◽  
Wang Shixuan ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Malignant Tumors ◽  
Chemotherapeutic Resistance ◽  
Novel Approach ◽  
Cervical Cancer Cells ◽  
Cancer Tissues

AbstractSema4C, the target of many miRNAs, is involved in EMT-mediated chemotherapeutic resistance of many malignant tumors. However, the underlying upstream regulatory mechanisms of Sema4C-induced EMT and Sema4C-mediated drug resistance are still unclear. The aim of this study was to explore the potential role of miR-31-3p/Sema4C in regulating EMT in cisplatin-resistant (CR) cervical cancer cells. High expression levels of Sema4C were more frequently found in cervical cancer tissues and were associated with poor prognosis, whereas miR-31-3p was significantly downregulated in cervical cancer tissues, which was associated with shorter disease-free and overall survival. Overexpression of miR-31-3p inhibited malignant behaviors and EMT of cervical cancer cells in vitro. Furthermore, miR-31-3p was identified to directly target Sema4C, and upregulation of miR-31-3p reversed EMT-mediated biological functions, including cisplatin resistance of Sema4C in cervical cancer cells. These results suggest that Sema4C promoted EMT-mediated cisplatin resistance in cervical cancer cells and that this effect was inhibited by overexpression of miR-31-3p. Thus, silencing Sema4C or overexpression of miR-31-3p could be a novel approach to treat drug resistance to chemotherapy in cervical cancers.

scholarly journals Nucleolin Promotes Cisplatin Resistance in Cervical Cancer by the YB1-MDR1 Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Jing Ke ◽  
Chunming Gu ◽  
Heyan Zhang ◽  
Yang Liu ◽  
Wenhao Zhang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Drug Resistance ◽  
Hela Cells ◽  
Protein Level ◽  
Molecular Mechanisms ◽  
Cisplatin Resistance ◽  
Mdr1 Gene ◽  
Luciferase Reporter ◽  
Drug Efflux ◽  
Cell Line Hela

Purpose. Cervical cancer is the fourth most common cancer in women worldwide and is the main cause of cancer-related deaths in women. Cisplatin (DDP) is one of the major chemotherapeutic drugs for cervical cancer patients. But, drug resistance limits the effectiveness of cancer therapy. Nucleolin (NCL) is a nucleocytoplasmic multifunctional protein involved in the development of cancer. It has been reported that NCL may be a potential target for modulation of drug resistance. However, the precise molecular mechanisms are poorly understood. Materials and Methods. Human cervical cancer Hela cells and their cisplatin-resistant cell line Hela/DDP were used in this study. The protein level of NCL in cervical cancer cells was measured by western blot analysis. Hela cells and Hela/DDP cells were transfected with NCL overexpression plasmid or NCL siRNA separately. MTT and EdU assay were performed to evaluate the cell viability and sensitivity to cisplatin. The drug efflux function of MDR1 protein was assessed by intracellular rhodamine-123 accumulation assay.The promoter activity of MDR1 was assessed by using a dual-luciferase reporter assay. Results. We found that the protein level of NCL was elevated in Hela/DDP cells. Overexpression of NCL increased cervical cancer cell proliferation and attenuated the sensitivity to cisplatin. Overexpression of NCL increased Multidrug resistance (MDR1) gene expression and drug efflux. Our results demonstrated that NCL was highly related with cisplatin resistance in cervical cancer. NCL played an important role in MDR1 gene transcription through regulation of the transcription factor YB1. Conclusion. Our findings revealed the novel role of NCL in cisplatin-resistant cervical cancer and NCL may be a potential therapeutic target for chemoresistance.

scholarly journals Research of the mechanism on miRNA193 in exosomes promotes cisplatin resistance in esophageal cancer cells

2019 ◽  
Author(s):  
Shifeng Shi ◽  
Xin Huang ◽  
Xiao Ma ◽  
Xiaoyan Zhu ◽  
Qinxian Zhang
Keyword(s):  
Cell Cycle ◽  
Drug Resistance ◽  
Esophageal Cancer ◽  
Cancer Cells ◽  
Tumor Cells ◽  
Cisplatin Resistance ◽  
High Expression ◽  
Drug Resistant ◽  
Cellular Resistance ◽  
Esophageal Cancer Cells

AbstractPurposeChemotherapy resistance of esophageal cancer is a key factor affecting the postoperative treatment of esophageal cancer. Among the media that transmit signals between cells, the exosomes secreted by tumor cells mediate information transmission between tumor cells, which can make sensitive cells obtain resistance. Although some cellular exosomes play an important role in tumor’s acquired drug resistance, the related action mechanism is still not explored specifically.MethodsTo elucidate this process, we constructed a cisplatin-resistant esophageal cancer cell line, and proved that exosomes conferring cellular resistance in esophageal cancer can promote cisplatin resistance in sensitive cells. Through high-throughput sequencing analysis of the exosome and of cells after stimulation by exosomes, we determined that the miRNA193 in exosomes conferring cellular resistance played a key role in sensitive cells acquiring resistance to cisplatin. In vitro experiments showed that miRNA193 can regulate the cell cycle of esophageal cancer cells and inhibit apoptosis, so that sensitive cells can acquire resistance to cisplatin. An in vivo experiment proved that miRNA193 can promote tumor proliferation through the exosomes, and provide sensitive cells with slight resistance to cisplatin.ResultsSmall RNA sequencing of exosomes showed that exosomes in drug-resistant cells have 189 up-regulated and 304 down-regulated miRNAs; transcriptome results showed that drug-resistant cells treated with drug-resistant cellular exosomes have 3446 high-expression and 1709 low-expression genes; correlation analysis showed that drug-resistant cellular exosomes mainly affect the drug resistance of sensitive cells through paths such as cytokine–cytokine receptor interaction, and the VEGF and Jak-STAT signaling pathways; miRNA193, one of the high-expression miRNAs in drug-resistant cellular exosomes, can promote drug resistance by removing cisplatin’s inhibition of the cell cycle of sensitive cells.ConclusionSensitive cells can become resistant to cisplatin through acquired drug-resistant cellular exosomes, and miRNA193 can make tumor cells acquire cisplatin resistance by regulating the cell cycle.

scholarly journals The Emerging Roles of Long Noncoding RNAs as Hallmarks of Lung Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Jun Jiang ◽  
Yuan Lu ◽  
Fang Zhang ◽  
Jie Huang ◽  
Xin-ling Ren ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Drug Resistance ◽  
Prognostic Markers ◽  
Chromatin Modification ◽  
Noncoding Rnas ◽  
Cancer Biomarkers ◽  
Mechanisms Of Action ◽  
Long Noncoding Rnas ◽  
Ribonucleic Acids ◽  
New Class

Noncoding ribonucleic acids (ncRNAs) are closely associated with tumor initiation, growth, and progress in lung cancer. Long ncRNAs (lncRNAs), as one of the three subclasses of ncRNAs, play important roles in chromatin modification, transcription, and post-transcriptional processing. Various lncRNAs have recently been reported to be dysfunctional or dysregulated in cancers and have pro- or anti-tumor potential. Importantly, as a new class of cancer biomarkers, studies have demonstrated the plausibility of using certain subsets of lncRNAs as promising diagnostic, therapeutic, or prognostic strategies to manage cancers. This review focuses on lncRNAs associated with hallmarks of lung cancer, especially those discovered in the last five years. The expression levels of these lncRNAs in tumor samples are discussed, alongside their mechanisms of action, drug resistance, and potential as diagnostic and prognostic markers for lung cancer.

scholarly journals Enhancer of mRNA Decapping protein 4 (EDC4) interacts with replication protein a (RPA) and contributes to Cisplatin resistance in cervical Cancer by alleviating DNA damage

Hereditas ◽  
2020 ◽  
Vol 157 (1) ◽  
Author(s):  
Xiaoling Wu ◽  
Youwen Zhong ◽  
Qing Chen ◽  
Xin Zhang ◽  
Hua Zhang
Keyword(s):  
Cervical Cancer ◽  
Dna Damage ◽  
Cell Growth ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Protein A ◽  
Replication Protein A ◽  
Replication Protein ◽  
Mrna Decapping ◽  
Cervical Cancer Cells

Abstract Background Cervical cancer (CC) is the third most common gynecological malignancy around the world. Cisplatin is an effective drug, but cisplatin resistance is a vital factor limiting the clinical usage of cisplatin. Enhancer of mRNA decapping protein 4 (EDC4) is a known regulator of mRNA decapping, which was related with genome stability and sensitivity of drugs. This research was to investigate the mechanism of EDC4 on cisplatin resistance in CC. Two human cervical cancer cell lines, HeLa and SiHa, were used to investigate the role of EDC4 on cisplatin resistance in vitro. The knockdown or overexpression of EDC4 or replication protein A (RPA) in HeLa or SiHa cells was performed by transfection. Cell viability was analyzed by MTT assay. The growth of cancer cells was evaluated by colony formation assay. DNA damage was measured by γH2AX (a sensitive DNA damage response marker) immunofluorescent staining. The binding of EDC4 and RPA was analyzed by immunoprecipitation. Results EDC4 knockdown in cervical cancer cells (HeLa and SiHa) enhanced cisplatin sensitivity and cisplatin induced cell growth inhibition and DNA damage. EDC4 overexpression reduced DNA damage caused by cisplatin and enhanced cell growth of cervical cancer cells. EDC4 could interact with RPA and promote RPA phosphorylation. RPA knockdown reversed the inhibitory effect of EDC4 on cisplatin-induced DNA damage. Conclusion The present results indicated that EDC4 is responsible for the cisplatin resistance partly through interacting with RPA in cervical cancer by alleviating DNA damage. This study indicated that EDC4 or RPA may be novel targets to combat chemotherapy resistance in cervical cancer. Graphical abstract

MiR-181a Promotes Apoptosis and Reduces Cisplatin Resistance by Inhibiting Osteopontin in Cervical Cancer Cells

2019 ◽  
Vol 34 (9) ◽  
pp. 559-565 ◽  
Author(s):  
Xiaofei Xu ◽  
Xiaofei Jiang ◽  
Liping Chen ◽  
Yu Zhao ◽  
Zhihua Huang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Cervical Cancer Cells
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