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论文题目: RNF216 contributes to proliferation and migration of colorectal cancer via suppressing BECN1-dependent autophagy
英文论文题目: RNF216 contributes to proliferation and migration of colorectal cancer via suppressing BECN1-dependent autophagy
第一作者: Wang, H; Wang, YA; Qian, L; Wang, X; Gu, HL; Dong, XQ; Huang, SQ; Jin, M; Ge, HL; Xu, CF; Zhang, YY
英文第一作者: Wang, H; Wang, YA; Qian, L; Wang, X; Gu, HL; Dong, XQ; Huang, SQ; Jin, M; Ge, HL; Xu, CF; Zhang, YY
联系作者: Xu, CF; Zhang, YY (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Key Lab Stem Cell Biol, Shanghai, Peoples R China.
英文联系作者: Xu, CF; Zhang, YY (reprint author), Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Key Lab Stem Cell Biol, Shanghai, Peoples R China.
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发表年度: 2016
卷: 7
期: 32
页码: 51174-51183
摘要: Originally identified as an E3 ligase regulating toll-like receptor (TLR) signaling, ring finger protein 216 (RNF216) also plays an essential role in autophagy, which is fundamental to cellular homeostasis. Autophagy dysfunction leads to an array of pathological events, including tumor formation. In this study, we found that RNF216 was upregulated in human colorectal cancer (CRC) tissues and cell lines, and was associated with progression of CRC. RNF216 promoted CRC cell proliferation and migration in vitro and in vivo, largely by enhancing proteasomal degradation of BECN1, a key autophagy regulator and tumor suppressor. RNF216 restricted CRC cell autophagy through BECN1 inhibition under nutritional starvation conditions. RNF216 knockdown increased the autophagy, limiting CRC cell proliferation and migration. Moreover, BECN1 knockdown or autophagy inhibition restored proliferation and migration of RNF216-knockdown CRC cells. Collectively, our results suggested that RNF216 promoted CRC cell proliferation and migration by negatively regulating BECN1-dependent autophagy. This makes RNF216 as a potential biomarker and novel therapeutic target for inhibiting CRC development and progression.
英文摘要: Originally identified as an E3 ligase regulating toll-like receptor (TLR) signaling, ring finger protein 216 (RNF216) also plays an essential role in autophagy, which is fundamental to cellular homeostasis. Autophagy dysfunction leads to an array of pathological events, including tumor formation. In this study, we found that RNF216 was upregulated in human colorectal cancer (CRC) tissues and cell lines, and was associated with progression of CRC. RNF216 promoted CRC cell proliferation and migration in vitro and in vivo, largely by enhancing proteasomal degradation of BECN1, a key autophagy regulator and tumor suppressor. RNF216 restricted CRC cell autophagy through BECN1 inhibition under nutritional starvation conditions. RNF216 knockdown increased the autophagy, limiting CRC cell proliferation and migration. Moreover, BECN1 knockdown or autophagy inhibition restored proliferation and migration of RNF216-knockdown CRC cells. Collectively, our results suggested that RNF216 promoted CRC cell proliferation and migration by negatively regulating BECN1-dependent autophagy. This makes RNF216 as a potential biomarker and novel therapeutic target for inhibiting CRC development and progression.
刊物名称: ONCOTARGET
英文刊物名称: ONCOTARGET
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学科: Oncology; Cell Biology
英文学科: Oncology; Cell Biology
影响因子: 5.168
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论文类别: Article
英文论文类别: Article
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