The Combination Therapy of Fluorouracil and Oxaliplatin Suppress the Progression of Colon Cancer Through miR-183-5p/SOCS3 Axis and Downregulating PD-L1.

PD-L1 SOCS3 colon cancer combination therapy miR-183-5p

Journal

Cancer management and research
ISSN: 1179-1322
Titre abrégé: Cancer Manag Res
Pays: New Zealand
ID NLM: 101512700

Informations de publication

Date de publication:
2021
Historique:
received: 15 09 2020
accepted: 20 01 2021
entrez: 4 3 2021
pubmed: 5 3 2021
medline: 5 3 2021
Statut: epublish

Résumé

The purpose of this study was to investigate the mechanism of combination of fluorouracil (FU) and oxaliplatin (OXA) on the progression of colon cancer via miR-183-5p/SOCS3 axis and regulating PD-L1. HCT116 cells were treated with 4 μM OXA and 10.5 μM FU, or exogenous regulation of the expression of miR-183-5p, SOCS3 and PD-L1 in HCT116 cells. CCK-8 assay was employed to detect cell viability of HCT116 cells. Flow cytometry was performed to assess the apoptosis and cell cycle. The expression level of SOCS3, PD-L1, chemokines (CCL1, CCL4 and CCL7) and immune escapes related proteins (EGFR, STARD1 and STARD3) in HCT116 cells were assessed by Western blotting. In addition, dual-luciferase reporter gene was carried out to verify the targeted relationship between miR-183-5p with SOCS3. Our study demonstrated that the combination of OXA and FU remarkably suppressed proliferation, promoted apoptosis and arrest cells in G0/G1 phrase of HCT116 cells, and observably downregulated the expression of PD-L1, CCL1, CCL4, CCL7, EGFR, STARD1 and STARD3. Meanwhile, the combination of OXA and FU significantly downregulated miR-183-5p expression. Knockdown of miR-183-5p also repressed the proliferation, promoted apoptosis and arrest cells in G0/G1 phrase of HCT116 cells, and downregulated the expression of PD-L1, CCL1, CCL4, CCL7, EGFR, STARD1 and STARD3. In addition, our study proved that miR-183-5p upregulated PD-L1 by targeting downregulated SOCS3 expression. Finally, we demonstrated that the combination therapy of OXA and FU inhibited the proliferation, promote apoptosis and arrest cells in G0/G1 phrase by downregulating PD-L1 via miR-183-5p/SOCS3 axis. The combination therapy of OXA and FU could suppress the malignant biological behavior, and the mechanism was realized by inhibiting PD-L1 through miR-183-5p/SOCS3 axis.

Identifiants

pubmed: 33658858
doi: 10.2147/CMAR.S281925
pii: 281925
pmc: PMC7920511
doi:

Types de publication

Journal Article

Langues

eng

Pagination

1999-2008

Informations de copyright

© 2021 Tu et al.

Déclaration de conflit d'intérêts

The authors report no conflicts of interest in this work.

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Auteurs

Changling Tu (C)

Department of Cadres Medical Oncology, The Third Affiliated Hospital of Kunming Medical University, Yunnan Cancer Hospital, Yunnan Cancer Center, Kunming, 650118, People's Republic of China.

Yufeng Wang (Y)

Department of Cadres Medical Oncology, The Third Affiliated Hospital of Kunming Medical University, Yunnan Cancer Hospital, Yunnan Cancer Center, Kunming, 650118, People's Republic of China.

Xianshuo Cheng (X)

Department of Colorectal Surgery, Third Affiliated Hospital, Kunming Medical University, Kunming, 650118, Yunnan, People's Republic of China.

Ying Zhu (Y)

Department of Cadres Medical Oncology, The Third Affiliated Hospital of Kunming Medical University, Yunnan Cancer Hospital, Yunnan Cancer Center, Kunming, 650118, People's Republic of China.

Wenli Yuan (W)

Department of Clinical Laboratory, The Fourth Affiliated Hospital of Kunming Medical University, Kunming, 650021, Yunnan, People's Republic of China.

Jian Dong (J)

The Third Affiliated Hospital of Kunming Medical University, Yunnan Cancer Hospital, Yunnan Cancer Center, Kunming, 650118, People's Republic of China.

Classifications MeSH