ABSTRACT Cisplatin (DDP) therapy is widely used for the treatment of non-small cell lung cancer (NSCLC), but the curative effect is limited by chemoresistance. This study was designed to explore circ_0020123 function in DDP resistance of NSCLCDDP. Expression detection for circ_0020123, microRNA-140-3p (miR-140-3p) and homeobox B5 (HOXB5) was performed by real-time polymerase chain reaction (qRT-PCR). Half inhibitory concentration (IC50) of DDP and cell proliferation was detected by Cell Counting Kit-8 (CCK-8) assay. Colony formation ability was assessed using colony formation assay. Cell migration and invasion were evaluated via transwell assay. Cell apoptosis was examined by flow cytometry. Protein analysis was conducted by Western blot. Dual-luciferase reporter assay was used to affirm target interaction. Circ_0020123 expression was upregulated in DDP-resistant NSCLC cells. DDP resistance was reduced by downregulation of circ_0020123 in NSCLC cells. Circ_0020123 was identified as a miR-140-3p sponge. The effect of si-circ_0020123 on DDP resistance was partly associated with miR-140-3p upregulation. HOXB5 was a downstream target for miR-140-3p. Overexpression of HOXB5 mitigated miR-140-3p-induced inhibition of DDP resistance in NSCLC cells. Circ_0020123 upregulated the level of HOXB5 partly via sponging miR-140-3p. Also, circ_0020123 promoted tumor growth in NSCLC/DDP xenografts by regulating miR-140-3p and HOXB5 levels at least in part. These results revealed that circ_0020123 promoted DDP resistance in NSCLC cells partly by targeting miR-140-3p/HOXB5 axis, indicating that circ_0020123 might be used as a molecular target in DDP treatment for NSCLC. Graphical Abstract

https://www.tandfonline.com/doi/pdf/10.1080/21655979.2022.2036910?needAccess=true

Circ_0020123 enhances the cisplatin resistance in non-small cell lung cancer cells partly by sponging miR-140-3p to regulate homeobox B5 (HOXB5)

Lung cancer is one of the high malignancy‐related incidence and mortality worldwide, accounting for about 13% of total cancer diagnoses. Currently, the use of anti‐cancer agents is still the main therapeutic method for lung cancer. However, cancer cells will gradually show resistance to these drugs with the progress of treatment. And the molecular mechanisms underlying chemotherapy agents resistance remain unclear. circRNAs are newly identified noncoding RNAs molecules with covalently closed circular structures. Previous studies have shown that circRNAs are associated with tumorigenesis and progression of various cancers, including lung cancer. Recently, growing reports have suggested that circRNAs could contribute to drug resistance of lung cancer cell through different mechanisms. Therefore, in this review, we summarized the functions and underlying mechanisms of circRNAs in regulating chemoresistance of lung cancer and discussed their potential applications for diagnosis, prognosis, and treatment of lung cancer.

Circular RNAs in chemotherapy resistance of lung cancer and their potential therapeutic application

Due to the characteristics of aggressiveness and high risk of postoperative recurrence, non-small cell lung cancer (NSCLC) is a serious hazard to human health, accounting for 85% of all lung cancer cases. Drug therapies, including chemotherapy, targeted therapy and immunotherapy, are effective treatments for NSCLC in clinics. However, most patients ultimately develop drug resistance, which is also the leading cause of treatment failure in cancer. To date, the mechanisms of drug resistance have yet to be fully elucidated, thus original strategies are developed to overcome this issue. Emerging studies have illustrated that circular RNAs (circRNAs) participate in the generation of therapeutic resistance in NSCLC. CircRNAs mediate the modulations of immune cells, cytokines, autophagy, ferroptosis and metabolism in the tumor microenvironment (TME), which play essential roles in the generation of drug resistance of NSCLC. More importantly, circRNAs function as miRNAs sponges to affect specific signaling pathways, directly leading to the generation of drug resistance. Consequently, this review highlights the mechanisms underlying the relationship between circRNAs and drug resistance in NSCLC. Additionally, several therapeutic drugs associated with circRNAs are summarized, aiming to provide references for circRNAs serving as potential therapeutic targets in overcoming drug resistance in NSCLC.

/pdf/the-emerging-role-of-circular-rnas-in-drug-resistance-of-non-etk5z8rl.pdf

The emerging role of circular RNAs in drug resistance of non-small cell lung cancer

This study assessed the value of circRNAs (circular RNAs) as prognostic markers in BC (breast cancer). We searched pertinent studies on the PubMed, Embase, and Web of Science online databases published according to PRISMA guidelines. A random-effects model for meta-analysis was used to assess the combined effect size of the HRs (hazard ratios) of the included studies. The heterogeneity test used Cochran's Q-test and I2 statistics. Thirty of the 520 trials retrieved were included in the systematic review. A total of 11 chemotherapeutic agents were used in the included studies. A total of 30 studies on 30 circRNAs were included in the systematic review. Of the 30 relevant circRNAs, 28 were upregulated and two were downregulated in breast cancer versus normal samples, and both were associated with increased drug resistance. Nine of 30 studies were used for the meta-analysis. The results of the meta-analysis showed that the groups with circRNA upregulation and circRNA downregulation showed the same prognostic risk (HR = 1.37, 95% Cl: 0.80-2.36, I2 = 63.7%). The results of subgroup analysis showed that both upregulated circRNAs (HR = 2.24, 95% Cl: 1.34-3.75, I2 = 0%) and downregulated circRNAs (HR = 0.61, 95% Cl: 0.45-0.83, I2 = 0%) were associated with poor BC prognosis. Collectively, the results of all relevant articles collected indicated that circRNAs showed good potential as possible clinical biomarkers of chemoresistance in BC patients. 

/pdf/current-evidence-on-circrnas-as-potential-theranostic-ly19ao9z.pdf

Current evidence on circRNAs as potential theranostic markers for detecting chemoresistance in breast cancer: a systematic review and meta‑analysis

Circular RNAs (circRNAs) have been shown to have critical roles in developing cancer and treatment resistance in an increasing body of research. The aim was to look into the functions and processes of hsa_circ_0003220 in the non-small cell lung cancer (NSCLC) chemoresistance. The NSCLC cell lines H460 and A549 were employed in present work. hsa_circ_0003220, miR-489-3p, and insulin-like growth factors (IGF1) mRNA levels were assessed with a quantitative real time polymerase chain reaction (qRT-PCR). The cisplatin, docetaxel, and paclitaxel (PTX) resistances were determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and the enzyme linked immunosorbent assay (ELISA) test measured IGF1 expression. In order to corroborate the miR-489-3p relation with hsa_circ_0003220 or IGF1, a dual-luciferase reporter method was applied. The level of hsa_circ_0003220 was raised in cells and tissues from PTX-resistant (PR) NSCLC. In PR NSCLC cells, hsa_circ_0003220 knockdown reduced chemoresistance. For the purpose of the mechanism study, hsa_circ_0003220 knockdown substantially reduced IGF1 expression via miR-489-3p sponging, reducing chemoresistance in PR NSCLC cells. By controlling the miR-489-3p/IGF1 axis, hsa_circ_0003220 knockdown helped NSCLC overcome chemoresistance, suggesting a potential circRNA-targeted therapy for the disease.

/pdf/hsa-circ-0003220-drives-chemoresistance-of-human-nsclc-cells-2d5ikzl2.pdf

Hsa_circ_0003220 Drives Chemoresistance of Human NSCLC Cells by Modulating miR-489-3p/IGF1

Cancer cell chemoresistance is the primary reason behind cancer treatment failure. Previous reports suggest that circular RNA (circRNA) hsa_circ_0074027 (HC0074027) is a crucial modulator of non-small cell lung cancer (NSCLC) disease progression. Herein, we delineated the underlying mechanism of HC0074027-regulated chemoresistance in NSCLC. We employed quantitative real-time polymerase chain reaction (qRT-PCR) or Elisa in the detection of HC0074027, micoRNA-379-5p (miR-379-5p), and insuline-like growth factor I (IGF1) expressions. Cell survival was evaluated via the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). Direct associations among HC0074027, miR-379-5p, and IGF1 were examined via dual-luciferase reporter (DLR) and RNA immunoprecipitation (RIP) assays. Lastly, HC0074027 was incorporated into nude mice to examine its biological activity in vivo. Based on our analysis, HC0074027 levels strongly correlated with NSCLC chemoresistance to docetaxel (DTX), cisplatin (DDP), and paclitaxel (PTX). Alternately, HC0074027 silencing enhanced chemosensitivity in vitro. In vivo, HC0074027 downregulation suppressed tumor expansion and increased cancer cell sensitivity to chemotherapy. We also revealed that HC0074027 physically interacts with miR-379-5p to exert its biological function in vitro. Moreover, IGF1 is a functionally crucial target of miR-379-5p in modulating NSCLC chemoresistance in vitro. Finally, we demonstrated that HC0074027 can indirectly modulate IGF1 levels via sequestering miR-379-5p. We demonstrated that HC0074027 promotes NSCLC chemoresistance via sequestering miR-379-5p activity, and modulating IGF1 expression. Our work highlights the significance of HC0074027 in NSCLC chemoresistance and suggests HC0074027 to be an excellent candidate for targeted NSCLC therapy.

Blocking hsa_circ_0074027 suppressed non-small cell lung cancer chemoresistance via the miR-379-5p/IGF1 axis.

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Blocking hsa_circ_0074027 suppressed non-small cell lung cancer chemoresistance via the miR-379-5p/IGF1 axis.