Modified TLR‐mediated downregulation of miR‐125b‐5p enhances CD248 (endosialin)‐induced metastasis and drug resistance in colorectal cancer cells

2019 ◽  
Vol 59 (2) ◽  
pp. 154-167 ◽  
Author(s):  
Ga‐Bin Park ◽  
Jee‐Yeong Jeong ◽  
Daejin Kim
Keyword(s):  
Colorectal Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Colorectal Cancer Cells

scholarly journals Anlotinib Overcomes Multiple Drug Resistant Colorectal Cancer Cells via Inactivating PI3K/AKT Pathway

2021 ◽  
Vol 21 ◽  
Author(s):  
Weilan Lan ◽  
Jinyan Zhao ◽  
Wujin Chen ◽  
Haixia Shang ◽  
Jun Peng ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Drug Resistance ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Akt Pathway ◽  
Inhibition Of Proliferation ◽  
Colorectal Cancer Cells ◽  
Induced Apoptosis

Background: Anlotinib is a multi-target tyrosine kinase inhibitor that has been reported to have activity against colorectal cancer. However, the mechanisms of how anlotinib mediates drug-resistance of colorectal cancer have not been fully described. Particularly the potential mechanisms regarding to the inhibition of proliferation and induction of apoptosis remain unknown. Objective: In this study, we intended to study the effect and related-mechanism of the proliferation, migration, invasion and induced apoptosis of anlotinib overcoming multidrug resistant colorectal cancer cells through in vitro experiments. Methods: Cell viability was determined by MTT assays and the resistant index was calculated. Colony formation and PI/RNase Staining were used for testing the proliferation of resistant cells. DAPI staining and Annexin V-FITC/PI staining were used to detect cell apoptosis. Migration and invasion were examined by transwell. Protein expression and activation of PI3K/AKT pathway were detected by western blot. LY294002 was used to verify whether anlotinib overcomes the drug-resistance of CRC cells by inactivating the PI3K/AKT pathway. Results: The results showed that the HCT-8/5-FU cells were resistant to multiple chemotherapy drugs (5-FU, ADM and DDP). Anlotinib significantly inhibited the cell viability, proliferation, migration, invasion and induced the cell apoptosis. Moreover, anlotinib downregulated the expression of survivin, cyclin D1, CDK4, caspase-3, Bcl-2, MMP-2, MMP-9, vimentin and N-cadherin, but up-regulated cleaved-caspase-3, Bax and E-cadherin and blocked the activity of the PI3K/AKT in HCT-8/5-FU cells. We found anlotinib and LY294002 overcame the drug resistance of HCT-8/5-FU cells by reducing the expression of PI3K/p-AKT. Conclusions: Anlotinib inhibited the proliferation, migration, invasion and induced apoptosis of HCT-8/5-FU cells, and the mechanisms may be that anlotinib conquered multidrug resistance of colorectal cancer cells via inactivating of PI3K/AKT pathway.

scholarly journals Curcumin Regulates ERCC1 Expression and Enhances Oxaliplatin Sensitivity in Resistant Colorectal Cancer Cells through Its Effects on miR-409-3p

2020 ◽  
Vol 2020 ◽  
pp. 1-16
Author(s):  
Wei Han ◽  
Hongli Yin ◽  
Hao Ma ◽  
Yi Wang ◽  
Desong Kong ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Resistance Mechanism ◽  
Cancer Cell Line ◽  
Colorectal Cancer Cell Line ◽  
Pcr Analysis ◽  
Colorectal Cancer Cells ◽  
Ercc1 Expression

Background. Oxaliplatin (L-OHP) resistance is a major obstacle to the effective treatment of colorectal cancer. The resistance mechanism(s) of colorectal tumors to L-OHP may be related to the regulation of ERCC1 by cancer-expressed miRNAs, but no in-depth studies on the miRNAs that affect drug resistance have been performed. Curcumin (Cur) can reverse the drug resistance of cancer cells, but its effects on ERCC1 expression and miRNA profiles in colorectal cancer have not been studied. Methods. To study the regulation effect of curcumin on ERCC1 expression and its effects on miRNAs, the L-OHP-resistant colorectal cancer cell line HCT116/L-OHP was established. MTT assays were used to evaluate cell proliferation. Flow cytometry was used to investigate apoptotic induction. Western blot and RT-PCR analysis were used to evaluate the expression of drug-associated ERCC1, Bcl-2, GST-π, MRP, P-gp, and survivin. Results. HCT116//L-OHP cell lines were successfully established. The combination of L-OHP and curcumin could reduce L-OHP resistance in vitro. In addition, combination therapy inhibited the expression of ERCC1, Bcl-2, GST-π, MRP, P-gp, and survivin at the mRNA and protein level. Curcumin was found to inhibit ERCC1 through its ability to modulate miR-409-3p. Conclusion. Curcumin can overcome L-OHP resistance in colorectal cancer cells through its effects on miR-409-3p mediated ERCC1 expression.

scholarly journals GSK-3β inhibitor 6-bromo-indirubin-3′-oxime promotes both adhesive activity and drug resistance in colorectal cancer cells

2017 ◽  
Vol 51 (6) ◽  
pp. 1821-1830 ◽  
Author(s):  
Kunping Liu ◽  
Jinbang Li ◽  
Xuefang Wu ◽  
Meixiang Chen ◽  
Feng Luo ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Colorectal Cancer Cells ◽  
Gsk 3Β

Loss of E-cadherin promotes the growth, invasion and drug resistance of colorectal cancer cells and is associated with liver metastasis

2012 ◽  
Vol 39 (6) ◽  
pp. 6707-6714 ◽  
Author(s):  
Xiaobing Chen ◽  
Yongsheng Wang ◽  
Hongping Xia ◽  
Qiwu Wang ◽  
Xiaochun Jiang ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Drug Resistance ◽  
Liver Metastasis ◽  
Cancer Cells ◽  
Colorectal Cancer Cells ◽  
E Cadherin

Su1164 EXPLOITING BIM DEPENDENCY OVERCOMES PD-L1-MEDIATED DRUG RESISTANCE IN COLORECTAL CANCER CELLS

2020 ◽  
Vol 158 (6) ◽  
pp. S-529-S-530
Author(s):  
Lei Sun ◽  
Arpad V. Patai ◽  
Bo Qin ◽  
Frank A. Sinicrope
Keyword(s):  
Colorectal Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Colorectal Cancer Cells

scholarly journals Bufalin reverses acquired drug resistance by inhibiting stemness in colorectal cancer cells

2017 ◽  
Vol 38 (3) ◽  
pp. 1420-1430 ◽  
Author(s):  
Jian Sun ◽  
Ke Xu ◽  
Yanyan Qiu ◽  
Hong Gao ◽  
Jianhua Xu ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Acquired Drug Resistance ◽  
Colorectal Cancer Cells
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