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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2018.1
- 수록면
- 894 - 907 (14page)
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Purpose Cancer-associated fibroblasts (CAFs) activated by cancer cells has a central role in development and malignant biological behavior in colorectal cancer (CRC). Adult fibroblasts do not express Snail, but Snail-positive fibroblasts are discovered in the stroma of malignant CRC and reported to be the key role to chemoresistance. However, the reciprocal effect of CAFs expressed Snail to chemoresistance on CRC cells and the underlying molecular mechanisms are not fully characterized. Materials and Methods Snail-overexpressed 3T3 stable cell lines were generated by lipidosome and CT26 mixed with 3T3-Snail subcutaneous transplanted CRC models were established by subcutaneous injection. Cell Counting Kit-8, flow cytometry and western blotting assays were performed, and immunohistochemistry staining was studied. The cytokines participated in chemoresistance was validated with reverse transcriptase-polymerase chain reaction and heatmap. Results Snail-expression fibroblasts are discovered in human and mouse spontaneous CRCs. Overexpression of Snail induces 3T3 fibroblasts transdifferentiation to CAFs. CT26 co-cultured with 3T3-Snail resisted the impairment from 5-fluorouracil and paclitaxel in vitro. The subcutaneous transplanted tumor models included 3T3-Snail cells develop without restrictions even after treating with 5-fluorouracil or paclitaxel. Moreover, these chemoresistant processes may be mediated by CCL1 secreted by Snail-expression fibroblasts via transforming growth factor /nuclear factor-B signaling pathways. Conclusion Taken together, Snail-expressing 3T3 fibroblasts display CAFs properties that support 5-fluorouracil and paclitaxel chemoresistance in CRC via participation of CCL1 and suggest that inhibition of the Snail-expression fibroblasts in tumor may be a useful strategy to limit chemoresistance.
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참고문헌 (27)
참고문헌 신청
Jemal A / 2011 / Global cancer statistics / CA Cancer J Clin 61:69~90
Yao J / 2017 / 53BP1 loss induces chemoresistance of colorectal cancer cells to 5-fluorouracil by inhibiting the ATM-CHK2-P53 pathway / J Cancer Res Clin Oncol 143:419~431
De Wever O / 2008 / Stromal myofibroblasts are drivers of invasive cancer growth / Int J Cancer 123:2229~2238
Kalluri R / 2016 / The biology and function of fibroblasts in cancer / Nat Rev Cancer 16:582~598
Piera-Velazquez S / 2011 / Role of endothelial-mesenchymal transition (EndoMT) in the pathogenesis of fibrotic disorders / Am J Pathol 179:1074~1080
Yao J / 2017 / 53BP1 loss induces chemoresistance of colorectal cancer cells to 5-fluorouracil by inhibiting the ATM-CHK2-P53 pathway / J Cancer Res Clin Oncol 143:419~431
De Wever O / 2008 / Stromal myofibroblasts are drivers of invasive cancer growth / Int J Cancer 123:2229~2238
Kalluri R / 2016 / The biology and function of fibroblasts in cancer / Nat Rev Cancer 16:582~598
Piera-Velazquez S / 2011 / Role of endothelial-mesenchymal transition (EndoMT) in the pathogenesis of fibrotic disorders / Am J Pathol 179:1074~1080
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