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. 2020 Mar 31;48(3):0300060520904847. doi: 10.1177/0300060520904847

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© The Author(s) 2020

Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 6. — MiR-34c regulates NSCLC chemosensitivity in vivo. (a) The mice were sacrificed and the tumor weights were measured. miR-34c mimics significantly suppressed the tumor weight. However, miR-34c ASO increased the tumor weight. Upregulated NOTCH1 expression significantly reversed the suppression of tumor growth by miR-34c mimics. (b) The IHC assay verified that miR-34c suppressed the expression of Ki67 but that NOTCH1 reversed it. (c) The correlation between miR-34c ASO and siNOTCH1 in regulating NSCLC chemotherapy resistance was analyzed in vivo. The combination of miR-34c inhibitor and paclitaxel or cisplatin treatment resulted in a significant decrease in tumor growth. Short hairpin RNAs specific to NOTCH1 (shNOTCH1) enhanced the inhibition of paclitaxel or cisplatin in the NSCLC xenograft model. (d) The IHC assay verified the expression of Ki67. When miR-34c was suppressed, the expression level of Ki67 was significantly lower in the shNOTCH1 combined with cisplatin or paclitaxel treatment group than in the control. (e) A schematic model showing that miR-34c-3p target inhibiting NOTCH1 suppresses the chemosensitivity and metastasis of NSCLC. miR, microRNA; NSCLC, non-small cell lung cancer; ASO, antisense oligonucleotides; IHC, immunohistochemistry. *p < 0.05.