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Start Over Author "Lin, Xiaobin" Topic colorectal cancer
6 results on '"Lin, Xiaobin"'

3. M2 macrophages confer resistance to 5-fluorouracil in colorectal cancer through the activation of CCL22/PI3K/AKT signaling

Author

Wei, Chen, Yang, Chaogang, Wang, Shuyi, Shi, Dongdong, Zhang, Chunxiao, Lin, Xiaobin, and Xiong, Bin

Subjects
chemotherapy resistance, M2 macrophages, colorectal cancer, 5-fluorouracil, CCL22, OncoTargets and Therapy, Original Research
Abstract

Chen Wei,1–4* Chaogang Yang,1–4* Shuyi Wang,1–4 Dongdong Shi,1–4 Chunxiao Zhang,1–4 Xiaobin Lin,1–4 Bin Xiong1–41Department of Gastrointestinal Surgery, Zhongnan Hospital of Wuhan University, Wuhan 430071, People’s Republic of China; 2Department of Gastric and Colorectal Surgical Oncology, Zhongnan Hospital of Wuhan University, Wuhan 430071, People’s Republic of China; 3Hubei Key Laboratory of Tumor Biological Behaviors, Wuhan 430071, People’s Republic of China; 4Hubei Cancer Clinical Study Center, Wuhan 430071, People’s Republic of China*These authors contributed equally to this workBackground: M2 macrophages are crucial components of tumor microenvironment that frequently associated with the resistance of therapeutic treatments in human cancers, but their role in the chemosensitivity of colorectal cancer (CRC) to 5-fluorouracil (5-FU) is still obscure.Methods: In our study, we clarified the biological functions of M2 macrophages and their mechanism on the chemosensitivity of CRC cells to 5-FU. Then, we analyzed the correlation between CCL22 and CD68+, and CD163+, tumor-associated macrophages (TAMs), and further elucidated the prognostic value of CCL22 and CD163+, M2 macrophages in clinical CRC samples.Results: M2 macrophages decreased the inhibitory effect of 5-FU on CRC cells migration and invasion by secreting CCL22, and declined the apoptosis induced by 5-FU. Treated with a neutralizing anti-CCL22 antibody destroyed these effects. We further illuminated that M2 macrophages regulated 5-FU resistance of CRC cells through epithelial-mesenchymal transition (EMT) program, PI3K/AKT pathway, and caspase-mediated apoptosis. Clinically, CCL22 was found to have elevated expression in CRC tissue samples, and was positively associated with CD163+, TAMs. Furthermore, the patients with higher CD163+, M2 macrophages and higher expression of CCL22 in CRC tissues had a lower overall survival (OS) rate compared with lower ones.Conclusion: Our findings indicate that M2 macrophage regulated 5-FU-mediated CRC chemoresistance via the EMT program, PI3K/AKT pathway, and caspase-mediated apoptosis by releasing CCL22.Keywords: M2 macrophages, colorectal cancer, 5-fluorouracil, chemotherapy resistance, CCL22

Published
2019

5. Correction to: miR-195-5p/NOTCH2-mediated EMT modulates IL-4 secretion in colorectal cancer to affect M2-like TAM polarization.

Author

Lin, Xiaobin, Wang, Shuyi, Sun, Min, Zhang, Chunxiao, Wei, Chen, Yang, Chaogang, Dou, Rongzhang, Liu, Qing, and Xiong, Bin

Subjects
*COLORECTAL cancer, *SECRETION
Abstract

In the original article [1], the terms 'osISET' and 'ISET' within the 'CTC capture' sub-section of the Materials and Methods section have both been replaced with 'CTCBIOPSY®'. [ABSTRACT FROM AUTHOR]

Published
2019
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6. miR-195-5p/NOTCH2-mediated EMT modulates IL-4 secretion in colorectal cancer to affect M2-like TAM polarization.

Author

Lin, Xiaobin, Wang, Shuyi, Sun, Min, Zhang, Chunxiao, Wei, Chen, Yang, Chaogang, Dou, Rongzhang, Liu, Qing, and Xiong, Bin

Subjects
*INTERSTITIAL cells, *COLORECTAL cancer, *CANCER cells, *TUMOR microenvironment, *SECRETION, *MACROPHAGES
Abstract

Background: Tumor microenvironment (TME) is a complex environment containing tumor cells, tumor-associated macrophages (TAMs), interstitial cells, and non-cellular components. Epithelial–mesenchymal transition (EMT), as a major actor in cancer tumorigenicity and metastasis, was involved in the interaction between TAMs and tumor cells. However, the potential mechanisms of EMT and how EMT-programmed tumor cells affect M2-like TAMs still need further exploration. Methods: An integrated analysis of nine CRC miRNA expression datasets was performed. Functional assays, including the EdU, clone formation, wound healing, and transwell assays, were used to determine the anticancer role of miR-195-5p in human CRC progression. Furthermore, RNA immunoprecipitation, RNA decay, and dual-luciferase reporter assays were used to determine the mechanism of miR-195-p CRC progression. Then co-culture, migration, and ELISA assays were applied to determine the role of miR-195-5p in macrophage recruitment and alternative polarization. Xenograft mouse models were used to determine the role of miR-195-5p in CRC tumorigenicity and TAM polarization in vivo. Results: An integrated analysis confirmed that miR-195-5p was significantly downregulated in CRC tissues, and patients with a low level of miR-195-5p had significantly shortened overall survival as revealed by the TCGA-COAD dataset. Altered miR-195-5p in colon cancer cells led to distinct changes of proliferation, migration, invasion, and EMT. Mechanistically, miR-195-5p regulated NOTCH2 expression in a post-transcriptional manner by directly binding to 3′-UTR of the Notch2 mRNA. Subsequently, miR-195-5p/NOTCH2 suppressed GATA3-mediated IL-4 secretion in CRC cells and ultimately inhibited M2-like TAM polarization. Conclusions: miR-195-5p may play a vital role in regulating NOTCH2-mediated tumor cell EMT, thereby affecting IL-4-related M2-like TAM polarization in CRC. [ABSTRACT FROM AUTHOR]

Published
2019
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