miR‐126‐5p enhances radiosensitivity of lung adenocarcinoma cells by inhibiting EZH2 via the KLF2/BIRC axis

Han, Fushi; Huang, Dongdong; Meng, Jinqian; Chu, Jiapeng; Wang, Meng; Chen, Shuzhen

doi:10.1111/jcmm.17135

Cited by 10 publications

(6 citation statements)

References 32 publications

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“…Wang et al clarified that miR‐218 promoted apoptosis of U2OS osteosarcoma cells by targeting BIRC5 32 . In addition, it has been reported that BIRC5 was the direct target of KLF2 and miR‐126‐5p could promote KLF2 expression to inhibit BIRC5 activation in lung adenocarcinoma cells 33 . In the current study, the potential binding site of KLF2 on the BIRC5 promoter region was identified and verified through ChIP analysis and dual‐luciferase reporter analysis.…”

Section: Discussionmentioning

confidence: 57%

“…32 In addition, it has been reported that BIRC5 was the direct target of KLF2 and miR‐126‐5p could promote KLF2 expression to inhibit BIRC5 activation in lung adenocarcinoma cells. 33 In the current study, the potential binding site of KLF2 on the BIRC5 promoter region was identified and verified through ChIP analysis and dual‐luciferase reporter analysis. The results indicate that KLF2 could suppress BIRC5 expression transcriptionally.…”

Section: Discussionmentioning

confidence: 78%

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miR‐92a‐3p promotes breast cancer proliferation by regulating the KLF2/BIRC5 axis

Chen

Zhou

et al. 2022

Thoracic Cancer

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Background Breast cancer remains the most common malignancy in females around the world. Recently, a growing number of studies have focused on gene dysregulation. In our previous study, Krüppel‐like factors (KLFs) were found to play essential roles in breast cancer development, among which KLF2 could function as a tumor suppressor. Nevertheless, the underlying molecular mechanism remains unclear. Methods miR‐92a‐3p was identified as the upstream regulator of KLF2 by starBase v.3.0. The regulation of KLF2 by miR‐92a‐3p was verified by a series of in vitro and in vivo assays. Further exploration revealed that Baculoviral IAP Repeat Containing 5 (BIRC5) was the target of KLF2. ChIP assay, dual‐luciferase reporter analysis, quantitative real‐time PCR, and western blot were performed for verification. Results miR‐92a‐3p functioned as a tumor promoter by inhibiting KLF2 by binding to its 3'‐untranslated region (3'‐UTR). In addition, KLF2 could transcriptionally suppress the expression of BIRC5. Conclusion Collectively, our results uncovered the miR‐92a‐3p/KLF2/BIRC5 axis in breast cancer and provided a potential mechanism for breast cancer development, which may serve as promising strategies for breast cancer therapy.

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Section: Discussionmentioning

confidence: 57%

Section: Discussionmentioning

confidence: 78%

miR‐92a‐3p promotes breast cancer proliferation by regulating the KLF2/BIRC5 axis

Chen

Zhou

et al. 2022

Thoracic Cancer

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“…We may speculate that IgG and IgM participate in humoral immunity, CD4 + is involved in regulating or assisting immune response, CD8 + can inhibit and kill T-lymphocytes. [23][24][25] EGFR-TKI targeted therapy only mildly affects the reproduction of normal tissue cells, and will not cause damage to normal tissues. Therefore, it has a small impact on the immune function of the body.…”

Section: Discussionmentioning

confidence: 99%

Effects of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) targeted combined chemotherapy on immune function, tumor markers and oxidative stress in patients with stage IV lung adenocarcinoma

Kun¹,

Wu²,

Chen

2023

Pak J Med Sci

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Objective: To investigate the effects of EGFR-TKI combined chemotherapy on immune function, tumor markers and oxidative stress in patients with stage-IV lung adenocarcinoma. Methods: This retrospective observational study included 116 patients with stage-IV lung adenocarcinoma, treated in The First Affiliated Hospital of Soochow University from January 2021 to January 2022. According to the treatment records, 60 patients that received pemetrexed + cisplatin for four courses were set as a Control-group and 56 patients that received EGFR-TKI + pemetrexed + cisplatin for four courses were set as an Observation-group. Changes in immune function, tumor marker levels and oxidative stress level in the two groups were analyzed and compared. Results: After the treatment, levels of CD3+, CD4+, IgG and IgM in the Control-group were significantly lower than those before the treatment. EGFR-TKI + pemetrexed + cisplatin resulted in levels of CD3+, CD4+, IgG and IgM higher than before the treatment, and compared to the Control-group (p<0.001). After the treatment, the levels of NSE, serum CEA, serum CA125, CYFEA21-1 in both groups were significantly lower than those before treatment, and lower in the Observation-group (p<0.001). After the treatment, VEGF and MMP9 levels in both groups were significantly lower than those before treatment, and markedly lower in the Observation-group (p<0.001). Conclusion: Compared with systemic chemotherapy, EGFR-TKI targeted combined chemotherapy for stage-IV lung adenocarcinoma is associated with enhanced immune function of patients. It more effectively inhibits the growth and proliferation of tumor cells and reduces the level of oxidative stress. doi: https://doi.org/10.12669/pjms.39.3.7397 How to cite this: Kun Y, Wu J, Chen S. Effects of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) targeted combined chemotherapy on immune function, tumor markers and oxidative stress in patients with stage IV lung adenocarcinoma. Pak J Med Sci. 2023;39(3):742-746. doi: https://doi.org/10.12669/pjms.39.3.7397 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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“…23 MiR-126-5p represses cell migration and facilitates apoptosis to enhance the radiosensitivity of LUAD cells through modulating the enhancer of zeste two polycomb repressive complex two subunit (EZH2)/Krüppel-like factor 2 (KLF2)/baculoviral IAP repeat containing 5 (BIRC5) axis. 24 Our bioinformatics analysis showed that miR-587 was sponged by A2M-AS1 and targeted by bone morphogenetic protein 3 (BMP3). Notably, miR-587 was previously discovered to be upregulated in NSCLC samples and closely linked to tumor staging, and miR-587 ehnanced the proliferative and migratory capabilities of NSCLC cells by downregulating cylindromatosis (CYLD).…”

Section: Introductionmentioning

confidence: 99%

Overexpression of lncRNA A2M-AS1 inhibits cell growth and aggressiveness via regulating the miR-587/bone morphogenetic protein 3 axis in lung adenocarcinoma

Guo

Peng

et al. 2022

Hum Exp Toxicol

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Lung adenocarcinoma (LUAD) is a malignant tumor that occurs in the lungs. Numerous reports have substantiated the participation of long non-coding RNAs (lncRNAs) in the tumorigenesis of LUAD. Previously, lncRNA alpha-2-macroglobulin antisense RNA 1 (A2M-AS1) was confirmed to be an important regulator in the biological processes of LUAD and dysregulation of A2M-AS1 was associated with non-small cell lung cancer (NSCLC) progression. However, the precise mechanism of A2M-AS1 in LUAD has not been elucidated. Therefore, our study was designed to investigate the detailed molecular mechanism of A2M-AS1 in LUAD. Herein, the expression of lncRNA A2M-AS1, microRNA (miRNA) miR-587, and bone morphogenetic protein 3 (BMP3) in LUAD cell lines and tissues were detected by real-time quantitative polymerase chain reaction (RT-qPCR) and western blotting. The viability, proliferation, migration and invasion of LUAD cells were tested by cell counting kit-8 (CCK-8), colony formation and Transwell assays. In vivo tumor growth was investigated by xenograft animal experiment. Interactions among A2M-AS1, miR-587 and BMP3 were measured by RNA pulldown and luciferase reporter assays. In this study, A2M-AS1 was downregulated in LUAD tissues and cells and related to poor prognosis in LUAD patients. A2M-AS1 overexpression suppressed LUAD cell proliferation, migration and invasion in vitro and inhibited tumor growth in vivo. Mechanistically, A2M-AS1 directly bound with miR-587 to promote BMP3 expression in LUAD cells. Low expression of BMP3 was found in LUAD tissues and cells and was closely correlated with poor prognosis in LUAD patients. BMP3 deficiency reserved the inhibitory influence of A2M-AS1 overexpression on LUAD cell behaviors. Overall, A2M-AS1 inhibits cell growth and aggressiveness via regulating the miR-587/BMP3 axis in LUAD.

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miR‐126‐5p enhances radiosensitivity of lung adenocarcinoma cells by inhibiting EZH2 via the KLF2/BIRC axis

Cited by 10 publications

References 32 publications

miR‐92a‐3p promotes breast cancer proliferation by regulating the KLF2/BIRC5 axis

miR‐92a‐3p promotes breast cancer proliferation by regulating the KLF2/BIRC5 axis

Effects of epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (TKIs) targeted combined chemotherapy on immune function, tumor markers and oxidative stress in patients with stage IV lung adenocarcinoma

Overexpression of lncRNA A2M-AS1 inhibits cell growth and aggressiveness via regulating the miR-587/bone morphogenetic protein 3 axis in lung adenocarcinoma

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