|
|
Effect of miR-567 and CacyBP on A549 cells of non-small cell lung cancer |
LI Haiyang1, ZHAO Zhenshan1, LI Jing1, RONG Yao1, ZHENG Aiming2, HAO Menghui1, TIAN Faming3 |
1. Kailuan General Hospital, Tangshan 063001, China; 2. Tangshan People's Hospital,Tangshan 063001, China; 3. North China University of Technology, Tangshan 063210, China |
|
|
Abstract Objective To investigate the effects of miR-567 and calcyin-binding protein (CacyBP) on proliferation, invasion and apoptosis of non-small cell lung cancer (NSCLC) A549 cells. Methods NSCLC A549 with high expression of miR-567 and CacyBP was selected as the study object. The experiment was divided into 4 groups, blank control group (NC group), transfected with pcDNA6.2 miR-567(si-miR-567 group). Transfected pcDNA6.2 CacyBP siRNA (si-CacyBP group) and pcDNA6.2 miR-567+CacyBP siRNA group (si-miR-567+CacyBP group); mRNA expressions of miR-567 and CacyBP were detected by qRT-PCR. Cell proliferation was detected by CCK-8 and MTT assay. Transwell assay was used to test cell migration and invasion. The apoptosis rate of NSCLC A549 cells was determined by flow cytometry. The changes of apoptotic proteins in each group were detected by Western bolt. Results Compared with NC group, the expression of miR-567 in si-miR-567 groupand si-miR-567+CacyBP group was significantly decreased. Compared with NC group, the CacyBP mRNA expression in si-CacyBP group and si-miR-567+CacyBP group was significantly decreased. The results of MTT assay showed that the cell proliferation inhibition rate of three groups was significantly higher than that of NC group, and the cell proliferation inhibition rate of si-miR-567+CacyBP group was significantly higher than that of si-miR-567 and si-CacyBP groups. The results of CCK-8 experiment showed that the cell proliferation count of three groups was significantly lower than that of NC group, and the cell proliferation count of si-miR-567+CacyBP group was significantly lower than that of si-miR-567 and si-CacyBP groups. Transwell experiment showed that the number of cell migration and invasion in NC group was significantly higher than that in si-miR-567 group, si-CacyBP group and si-miR-567+CacyBP group. The number of cell migration and invasion in si-miR-567 group and si-CacyBP group was significantly higher than that in si-miR-567+CacyBP group. Flow cytometry showed that compared with NC group, the apoptosis rate of A549 cells in si-miR-567 group, si-CacyBP group and si-miR-567+CacyBP group was significantly increased. The apoptosis rate of A549 cells in si-miR-567+CacyBP group was significantly higher than that in si-miR-567 and si-CacyBP groups. Conclusion Combined intervention of miR-567 and CacyBP can effectively reduce the proliferation, migration and invasion ability of NSCLC A549 cells, and increase the apoptosis rate of cells.
|
Received: 27 October 2023
|
|
|
|
|
[1] ALEXANDER M, KIM SY, CHENG H.Update 2020: Management of Non-Small Cell Lung Cancer[J]. Lung, 2020, 198(6): 897-907. [2] DUMA N, SANTANA-DAVILA R, MOLINA JR.Non-Small Cell Lung Cancer: Epidemiology, Screening, Diagnosis, and Treatment[J]. Mayo Clin Proc, 2019, 94(8): 1623-1640. [3] LIANG G, MENG W, HUANG X, et al.miR-196b-5p-mediated downregulation of TSPAN12 and GATA6 promotes tumor progression in non-small cell lung cancer[J]. Proc Natl Acad Sci U S A, 2020, 117(8): 4347-4357. [4] NI J, ZHANG X, LI J, et al.Tumour-derived exosomal lncRNA-SOX2OT promotes bone metastasis of non-small cell lung cancer by targeting the miRNA-194-5p/RAC1 signalling axis in osteoclasts[J]. Cell Death Dis, 2021, 12(7): 662. [5] HAN M, HU J, LU P, et al.Exosome-transmitted miR-567 reverses trastuzumab resistance by inhibiting ATG5 in breast cancer[J]. Cell Death Dis, 2020, 11(1): 43. [6] 张婷, 赵顺玉, 孔双喜. miR-567在胰腺癌细胞中的表达及其作用机制[J]. 中国普通外科杂志, 2017, 26(9): 1141-1147. [7] PENG Y, LIU C, LI M, et al.Identification of a prognostic and therapeutic immune signature associated with hepatocellular carcinoma[J]. Cancer Cell Int, 2021, 21(1): 98. [8] CHEN X, ZHENG P, XUE Z, et al.CacyBP/SIP enhances multidrug resistance of pancreatic cancer cells by regulation of P-gp and Bcl-2[J]. Apoptosis, 2013, 18(7): 861-869. [9] RUIZ-CORDERO R, DEVINE WP.Targeted Therapy and Checkpoint Immunotherapy in Lung Cancer[J]. Surg Pathol Clin, 2020, 13(1): 17-33. [10] BADE BC, DELA CRUZ CS.Lung Cancer 2020: Epidemiology, Etiology, and Prevention[J]. Clin Chest Med, 2020, 41(1): 1-24. [11] CORRALES L, ROSELL R, CARDONA AF, et al.Lung cancer in never smokers: The role of different risk factors other than tobacco smoking[J]. Crit Rev Oncol Hematol, 2020, 148(1): 102895. [12] HOWLADER N, FORJAZ G, MOORADIAN MJ, et al.The Effect of Advances in Lung-Cancer Treatment on Population Mortality[J]. N Engl J Med, 2020, 383(7): 640-649. [13] RUIZ-CORDERO R, DEVINE WP.Targeted Therapy and Checkpoint Immunotherapy in Lung Cancer[J]. Surg Pathol Clin, 2020, 13(1): 17-33. [14] RECK M, CARBONE DP, GARASSINO M, et al.Targeting KRAS in non-small-cell lung cancer: recent progress and new approaches[J]. Ann Oncol, 2021, 32(9): 1101-1110. [15] ZHANG F, LI K, YAO X, et al.A miR-567-PIK3AP1-PI3K/AKT-c-Myc feedback loop regulates tumour growth and chemoresistance in gastric cancer[J]. EBioMedicine, 2019, 44(1): 311-321. [16] HAN M, HU J, LU P, et al.Exosome-transmitted miR-567 reverses trastuzumab resistance by inhibiting ATG5 in breast cancer[J]. Cell Death Dis, 2020, 11(1): 43. [17] MENZL I, WITALISZ-SIEPRACKA A, SEXL V.CDK8-Novel Therapeutic Opportunities[J]. Pharmaceuticals (Basel), 2019, 12(2): 92. [18] GRACZYK-JARZYNKA A, SOBIAK B, MLĄCKI M, et al. S100A6 activates EGFR and its downstream signaling in HaCaT keratinocytes[J]. J Cell Physiol, 2019, 234(10): 17561-17569. [19] ROSIŃSKA S, LEŚNIAK W, FILIPEK A. Distinct effect of CacyBP/SIP on the ERK1/2-CREB-BDNF pathway in undifferentiated and differentiated neuroblastoma NB2a cells[J]. Neurochem Int, 2016, 97: 65-72. [20] XU YJ, HU YM, QIN C, et al.[CacyBP promotes the proliferation and invasion of non-small cell lung cancer][J]. Zhonghua Zhong Liu Za Zhi, 2021, 43(9): 924-931. |
|
|
|