circ_103809 promotes breast cancer progression by regulating the PI3K/AKT signaling pathway

Qiu, Xiaoli; Wang, Qinghua; Song, Huiping; Шао, Ди; Xue, Jie

doi:10.3892/ol.2020.11507

Cited by 21 publications

(19 citation statements)

References 15 publications

(15 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Furthermore, upregulation of hsa_circRNA_103809 increased cisplatin-resistance in CS-NSCLC cells, implying that targeting hsa_circRNA_103809 could potentially improve cisplatin-sensitivity in NSCLC cells. Previous data suggested that hsa_circRNA_103809 acted as an oncogene to promote cancer progression [15,19,18,16,17] , and this study evidenced that hsa_circRNA_103809 also modulated drug resistance in NSCLC, which broadened our knowledge in this eld.…”

Section: Discussionsupporting

confidence: 65%

A novel circular RNA hsa_circRNA_103809/miR-377-3p/GOT1 pathway regulates cisplatin-resistance in non-small cell lung cancer (NSCLC)

Zhu

Han

Lan

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Cisplatin is the first-line chemotherapeutic drug for non-small cell lung cancer (NSCLC), and emerging evidences suggests that targeting circular RNAs (circRNAs) is an effective strategy to increase cisplatin-sensitivity in NSCLC, but the detailed mechanisms are still not fully delineated. Methods: Cell proliferation, viability and apoptosis were examined by using the cell counting kit-8 (CCK-8) assay, trypan blue staining assay and Annexin V-FITC/PI double staining assay, respectively. The expression levels of cancer associated genes were measured by using the Real-Time qPCR and Western Blot analysis at transcriptional and translated levels. Dual-luciferase reporter gene system assay was conducted to validated the targeting sites among hsa_circRNA_103809, miR-377-3p and 3’ untranslated region (3’UTR) of GOT1 mRNA. The expression status, including expression levels and localization, were determined by immunohistochemistry (IHC) assay in mice tumor tissues.Results: Here we identified a novel hsa_circRNA_103809/miR-377-3p/GOT1 signaling cascade which contributes to cisplatin-resistance in NSCLC in vitro and in vivo. Mechanistically, parental cisplatin-sensitive NSCLC (CS-NSCLC) cells were subjected to continuous low-dose cisplatin treatment to generate cisplatin-resistant NSCLC (CR-NSCLC) cells, and we found that hsa_circRNA_103809 and GOT1 were upregulated, while miR-377-3p was downregulated in CR-NSCLC cells but not in CS-NSCLC cells. In addition, hsa_circRNA_103809 sponged miR-337-3p to upregulate GOT1 in CS-NSCLC cells, and knock-down of hsa_circRNA_103809 enhanced the inhibiting effects of cisplatin on cell proliferation and viability, and induced cell apoptosis in CR-NSCLC cells, which were reversed by downregulating miR-377-3p and overexpressing GOT1. Consistently, overexpression of hsa_circRNA_103809 increased cisplatin-resistance in CS-NSCLC cells by regulating the miR-377-3p/GOT1 axis. Finally, silencing of hsa_circRNA_103809 aggravated the inhibiting effects of cisplatin treatment on NSCLC cell growth in vivo. Conclusions: Analysis of data suggested that targeting the hsa_circRNA_103809/miR-377-3p/GOT1 pathway increased susceptibility of CR-NSCLC cells to cisplatin, and this study provided novel targets to improve the therapeutic efficacy of cisplatin for NSCLC treatment in clinic.

show abstract

Section: Discussionsupporting

confidence: 65%

A novel circular RNA hsa_circRNA_103809/miR-377-3p/GOT1 pathway regulates cisplatin-resistance in non-small cell lung cancer (NSCLC)

Zhu

Han

Lan

et al. 2020

Preprint

View full text Add to dashboard Cite

show abstract

“…Consistently, upregulation of hsa_circRNA_103809 increased cisplatin-resistance in CS-NSCLC cells, implying that targeting hsa_circRNA_103809 was feasible to improve cisplatin-sensitivity in NSCLC cells. Previous data suggested that hsa_circRNA_103809 acted as an oncogene to promote cancer progression [14][15][16][17][18], and this study evidenced that hsa_circRNA_103809 also modulated drug resistance in NSCLC, which broadened our knowledge in this eld.…”

Section: Discussionsupporting

confidence: 60%

“…Recently, researchers found that continuous long-term cisplatin stimulation caused alteration of multiple cancer associated Circular RNAs (circRNAs) in NSCLC cells, resulting in cisplatin-resistance in cancer cells, which made cisplatin "ineffectiveness" to eliminate NSCLC cells [12,13], and uncovering the underlying mechanisms might solve this problem. Based on the above information, by searching the online Pubmed database (https://pubmed.ncbi.nlm.nih.gov/), we selected hsa_circRNA_103809 for further investigations in this study, and the main reason is that hsa_circRNA_103809 acted as an oncogene to promote cancer development in colorectal cancer [14], breast cancer [15], hepatocellular carcinoma [16], gastric cancer [17] and lung cancer [18]. However, up until now, the role of hsa_circRNA_103809 in regulating drug resistance in cancer treatment is still largely unknown, which made this issue become valuable and meaningful.…”

Section: Introductionmentioning

confidence: 99%

A novel circular RNA hsa_circRNA_103809/miR-377-3p/GOT1 pathway regulates cisplatin-resistance in non-small cell lung cancer (NSCLC)

Zhu

Han

Lan

et al. 2020

Preprint

View full text Add to dashboard Cite

Background Cisplatin is the first-line chemotherapeutic drug for non-small cell lung cancer (NSCLC), and emerging evidences suggests that targeting circular RNAs (circRNAs) is an effective strategy to increase cisplatin-sensitivity in NSCLC, but the detailed mechanisms are still not fully delineated. Methods Cell proliferation, viability and apoptosis were examined by using the cell counting kit-8 (CCK-8) assay, trypan blue staining assay and Annexin V-FITC/PI double staining assay, respectively. The expression levels of cancer associated genes were measured by using the Real-Time qPCR and Western Blot analysis at transcriptional and translated levels. Dual-luciferase reporter gene system assay was conducted to validated the targeting sites among hsa_circRNA_103809, miR-377-3p and 3’ untranslated region (3’UTR) of GOT1 mRNA. The expression status, including expression levels and localization, were determined by immunohistochemistry (IHC) assay in mice tumor tissues. Results Here we identified a novel hsa_circRNA_103809/miR-377-3p/GOT1 signaling cascade contributes to cisplatin-resistance in NSCLC in vitro and in vivo. Mechanistically, parental cisplatin-sensitive NSCLC (CS-NSCLC) cells were subjected to continuous low-dose cisplatin treatment to generate cisplatin-resistant NSCLC (CR-NSCLC) cells, and we found that hsa_circRNA_103809 and GOT1 were upregulated, while miR-377-3p was downregulated in CR-NSCLC cells but not in CS-NSCLC cells. In addition, hsa_circRNA_103809 sponged miR-337-3p to upregulate GOT1 in CS-NSCLC cells, and knock-down of hsa_circRNA_103809 enhanced the inhibiting effects of cisplatin on cell proliferation and viability, and induced cell apoptosis in CR-NSCLC cells, which were reversed by downregulating miR-377-3p and overexpressing GOT1. Consistently, overexpression of hsa_circRNA_103809 increased cisplatin-resistance in CS-NSCLC cells by regulating the miR-377-3p/GOT1 axis. Finally, silencing of hsa_circRNA_103809 aggravated the inhibiting effects of cisplatin treatment on NSCLC cell growth in vivo. Conclusions Analysis of data suggested that targeting the hsa_circRNA_103809/miR-377-3p/GOT1 pathway increased susceptibility of CR-NSCLC cells to cisplatin, and this study provided novel targets to improve the therapeutic efficacy of cisplatin for NSCLC treatment in clinic.

show abstract

“…*P < 0.05 cisplatin-resistance in CS-NSCLC cells, implying that targeting hsa_circRNA_103809 could potentially improve cisplatin-sensitivity in NSCLC cells. Previous data suggested that hsa_circRNA_103809 acted as an oncogene to promote cancer progression [15][16][17][18][19], and this study evidenced that hsa_circRNA_103809 also modulated drug resistance in NSCLC, which broadened our knowledge in this field.…”

Section: Discussionsupporting

confidence: 59%

“…Uncovering the underlying mechanisms leading to this resistance might solve this problem. Based on the above information, by searching the online Pubmed database (https://pubmed.ncbi.nlm.nih.gov/), we selected hsa_circRNA_103809 for further investigations in this study, and the main reason is that hsa_circRNA_103809 acted as an oncogene to promote cancer development in colorectal cancer [15], breast cancer [16], hepatocellular carcinoma [17], gastric cancer [18] and lung cancer [19]. However, to date, the role of hsa_circRNA_103809 in drug resistance in cancer remains largely unknown and therefore important to investigate.…”

Section: Introductionmentioning

confidence: 99%

A novel circular RNA hsa_circRNA_103809/miR-377-3p/GOT1 pathway regulates cisplatin-resistance in non-small cell lung cancer (NSCLC)

et al. 2020

View full text Add to dashboard Cite

Background Cisplatin is the first-line chemotherapeutic drug for non-small cell lung cancer (NSCLC), and emerging evidences suggests that targeting circular RNAs (circRNAs) is an effective strategy to increase cisplatin-sensitivity in NSCLC, but the detailed mechanisms are still not fully delineated. Methods Cell proliferation, viability and apoptosis were examined by using the cell counting kit-8 (CCK-8) assay, trypan blue staining assay and Annexin V-FITC/PI double staining assay, respectively. The expression levels of cancer associated genes were measured by using the Real-Time qPCR and Western Blot analysis at transcriptional and translated levels. Dual-luciferase reporter gene system assay was conducted to validated the targeting sites among hsa_circRNA_103809, miR-377-3p and 3′ untranslated region (3’UTR) of GOT1 mRNA. The expression status, including expression levels and localization, were determined by immunohistochemistry (IHC) assay in mice tumor tissues. Results Here we identified a novel hsa_circRNA_103809/miR-377-3p/GOT1 signaling cascade which contributes to cisplatin-resistance in NSCLC in vitro and in vivo. Mechanistically, parental cisplatin-sensitive NSCLC (CS-NSCLC) cells were subjected to continuous low-dose cisplatin treatment to generate cisplatin-resistant NSCLC (CR-NSCLC) cells, and we found that hsa_circRNA_103809 and GOT1 were upregulated, while miR-377-3p was downregulated in CR-NSCLC cells but not in CS-NSCLC cells. In addition, hsa_circRNA_103809 sponged miR-337-3p to upregulate GOT1 in CS-NSCLC cells, and knock-down of hsa_circRNA_103809 enhanced the inhibiting effects of cisplatin on cell proliferation and viability, and induced cell apoptosis in CR-NSCLC cells, which were reversed by downregulating miR-377-3p and overexpressing GOT1. Consistently, overexpression of hsa_circRNA_103809 increased cisplatin-resistance in CS-NSCLC cells by regulating the miR-377-3p/GOT1 axis. Finally, silencing of hsa_circRNA_103809 aggravated the inhibiting effects of cisplatin treatment on NSCLC cell growth in vivo. Conclusions Analysis of data suggested that targeting the hsa_circRNA_103809/miR-377-3p/GOT1 pathway increased susceptibility of CR-NSCLC cells to cisplatin, and this study provided novel targets to improve the therapeutic efficacy of cisplatin for NSCLC treatment in clinic.

show abstract

circ_103809 promotes breast cancer progression by regulating the PI3K/AKT signaling pathway

Abstract: Breast cancer is one of the most common cancer types in the world. This study was carried out to investigate the functional role of circular RNA circ_103809 in breast cancer.

Cited by 21 publications

References 15 publications

A novel circular RNA hsa_circRNA_103809/miR-377-3p/GOT1 pathway regulates cisplatin-resistance in non-small cell lung cancer (NSCLC)

A novel circular RNA hsa_circRNA_103809/miR-377-3p/GOT1 pathway regulates cisplatin-resistance in non-small cell lung cancer (NSCLC)

A novel circular RNA hsa_circRNA_103809/miR-377-3p/GOT1 pathway regulates cisplatin-resistance in non-small cell lung cancer (NSCLC)

A novel circular RNA hsa_circRNA_103809/miR-377-3p/GOT1 pathway regulates cisplatin-resistance in non-small cell lung cancer (NSCLC)

Contact Info

Product

Resources

About