期刊：
CURRENT MOLECULAR PHARMACOLOGY,2020年13(1):31-40 ISSN：1874-4672
通讯作者：
He, Xiu-sheng
作者机构：
[He, Xiu-sheng; Liu, Wen-Ling; Li, Lei; Su, Lei] Univ South China, Hengyang Med Coll, Canc Res Inst, 28 West Changsheng Rd, Hengyang City, Hunan, Peoples R China.;[Lu, Zhou-cheng] Univ South China, Affiliated Hosp 2, Hengyang City, Hunan, Peoples R China.
通讯机构：
[He, Xiu-sheng] U;Univ South China, Hengyang Med Coll, Canc Res Inst, 28 West Changsheng Rd, Hengyang City, Hunan, Peoples R China.
期刊：
Frontiers in Genetics,2020年10:501407 ISSN：1664-8021
通讯作者：
He, Xiu-Sheng;Liu, Wen;Ye, Feng
作者机构：
[He, Xiu-Sheng; Tang, Guo-Hui] Univ South China, Hunan Prov Key Lab Canc Cellular & Mol Pathol, Hengyang, Peoples R China.;[He, Xiu-Sheng; Tang, Guo-Hui] Univ South China, Canc Res Inst, Hengyang Med Coll, Hengyang, Peoples R China.;[Tang, Guo-Hui] Univ South China, Dept Anus & Bowels, Affiliated Nanhua Hosp, Hengyang, Peoples R China.;[Du, Jun; Ding, Jian-Cheng; Liu, Wen; Chen, Xue] Xiamen Univ, Fujian Prov Key Lab Innovat Drug Target Res, Sch Pharmaceut Sci, Xiamen, Peoples R China.;[Xia, Lu; Lian, Jia-Bian; Lin, Xiao-Ting; Ye, Feng] Xiamen Univ, Dept Med Oncol, Affiliated Hosp 1, Xiamen, Peoples R China.
通讯机构：
[He, Xiu-Sheng] U;[Liu, Wen; Ye, Feng] X;Univ South China, Hunan Prov Key Lab Canc Cellular & Mol Pathol, Hengyang, Peoples R China.;Univ South China, Canc Res Inst, Hengyang Med Coll, Hengyang, Peoples R China.;Xiamen Univ, Fujian Prov Key Lab Innovat Drug Target Res, Sch Pharmaceut Sci, Xiamen, Peoples R China.
关键词：
cell growth;colorectal cancer;long non-coding RNA;therapeutic target;unfolded protein response
摘要：
Colorectal cancer (CRC) is the second most common cause of cancer-related death worldwide, and is well known for its strong invasiveness, rapid recurrence, and poor prognosis. Long non-coding RNAs (lncRNAs) have been shown to be involved in the development of various types of cancers, including colorectal cancer. Here, through transcriptomic analysis and functional screening, we reported that lncRNA LUCRC (LncRNA Upregulated in Colorectal Cancer) is highly expressed in colorectal tumor samples and is required for colorectal cancer cell proliferation, migration, and invasion in cultured cells and tumorigenesis in xenografts. LUCRC was found to regulate target gene expression of unfolded protein response (UPR) in endoplasmic reticulum (ER), such as BIP. The clinical significance of LUCRC is underscored by the specific presence of LUCRC in blood plasma of patients with colorectal cancers. These findings revealed a critical regulator of colorectal cancer development, which might serve as a therapeutic target in colorectal cancer.
关键词：
breast cancer;circular RNAs;competitive endogenous RNAs;metastasis
摘要：
Increasing studies have revealed that circular RNAs (circRNAs) play important roles in cancer progression. However, the potential involvement of circRNAs in breast cancer metastasis to lung is not clear so far. In this study, we conducted circular RNA microarrays of primary breast cancer tissues and lung metastatic tissues. The results revealed that circFBXL5 (hsa_circ_0125597) up-regulated the most in lung metastatic tissues. Survival analysis revealed that high levels of circFBXL5 correlated with worse outcome of breast cancer. Further experiments showed that knockdown of circFBXL5 inhibited breast cancer cell proliferation and migration to lung. Mechanism study showed that circFBXL5 acted as a sponge for miR-660 and compete binding to miR-660 with SRSF6, leading to increased expression of SRSF6. Collectively, our study highlighted the regulatory function of the circFBXL5/miR-660/SRSF6 pathway in breast cancer progression, which could be potential therapeutic targets for breast cancer.
期刊：
Cancer Letters,2017年403:175-185 ISSN：0304-3835
通讯作者：
Liu, Hao;He, Zhimin
作者机构：
[Liu, Hao; Zhang, Ruixin; Zheng, Guopei; Jia, Xiaoting; Deng, Min; Qiu, Qinwei; He, Zhimin; Liu, H] Guangzhou Med Univ, Canc Hosp, Guangzhou, Guangdong, Peoples R China.;[Liu, Hao; Zhang, Ruixin; Zheng, Guopei; Jia, Xiaoting; Deng, Min; Qiu, Qinwei; He, Zhimin; Liu, H] Guangzhou Med Univ, Canc Res Inst, Guangzhou, Guangdong, Peoples R China.;[Zeng, Chao] Guangdong Med Univ, Dept Pathol, Dongguan, Guangdong, Peoples R China.;[Lu, Xihong] Guangzhou Eighth Peoples Hosp, Guangzhou, Guangdong, Peoples R China.;[He, Xiusheng] Univ South China, Canc Res Inst, Hengyang, Hunan, Peoples R China.
通讯机构：
[Liu, H; He, ZM] G;Guangzhou Med Univ, Canc Hosp, Guangzhou, Guangdong, Peoples R China.;Guangzhou Med Univ, Canc Res Inst, Guangzhou, Guangdong, Peoples R China.
关键词：
miR-218;E2F1;CDK6;Cyclin D1;Gastric cancer
摘要：
Studies in several cancers have suggested that miR-218 has anti-tumor activities, but its function is yet to be elucidated. In this study, we investigated the regulation and function of miR-218 (miR-218-5p) in the cell cycle progression of gastric cancer (GC). We found that miR-218 could suppress proliferation of gastric cancer cells, induce cell cycle arrest at the G1 phase and inhibit tumor growth and metastasis in vivo. We also demonstrated that miR-218 specifically targeted the 3'-UTR regions of CDK6 and cyclin D1 and inhibited the expression of these molecules, which in turn repressed the pRb/E2F1 signaling pathway. Overexpression of CDK6 and Cyclin Dl reversed miR-218-mediated inhibition of pRI3/E2F1 signaling and attenuated the miR-218-induced cell cycle arrest. More importantly, miR-218 expression was significantly reduced and inversely correlated with the levels of CDK6 and Cyclin Dl in gastric cancer tissues. Decreased miR-218 expression was also correlated with advanced clinical stage, lymph node metastasis, and poor prognosis in gastric cancer patients. Furthermore, we showed that miR-218 expression was directly activated by E2F1 through the transactivation of miR-218 host genes, SLIT2 and SLIT3, revealing a negative feedback regulation of miR-218 expression. Taken together, our results describe a regulatory loop miR-218-CDK6/CyclinD1-E2F1 whose disruption may contribute to cell cycle progression in gastric cancer and indicate the potential application of miR-218 in cancer therapy. (C) 2017 Elsevier B.V. All rights reserved.
期刊：
中国全科医学,2017年20(17):2085-2088 and 2094 ISSN：1007-9572
通讯作者：
He, X.-S.
作者机构：
[汤国辉; 刑佼涛] Department of Anus and Bowels, Affiliated Nanhua Hospital, University of South China, Hengyang, 421002, China;[张志伟; 贺修胜; 谢运杰; 黄卫国] Cancer Research Institute, University of South China, Hengyang, 421001, China
通讯机构：
[He, X.-S.] C;Cancer Research Institute, University of South China, Hengyang, China
摘要：
Osteosarcoma (OS) is an aggressive malignant tumor that is mesenchymal in origin with a very low 5-year survival rate, particularly in the patients with locally advanced or metastatic tumors and recurrent disease. MicroRNAs (miRNAs) play a critical role in essential biological processes as cellular proliferation, differentiation and apoptosis in normal or cancer cells, including OS cells. In the present study, we aimed to investigate the role of miR-422a in OS. We demonstrated that miR-422a expression was significantly downregulated in OS tissues and cell lines compared with the normal controls. In addition, overexpression of miR-422a was able to inhibit cell proliferation and the ability of invasion, and enhance paclitaxel and cisplatin-mediated apoptosis in OS cells. Inversely, downregulation of miR-422a exhibited an opposite role. We further demonstrated that miR-422a directly targeted TGF beta 2 and regulated its expression and the activation of downstream molecules, smad2 and smad3 in OS cells. Thus, miR-422a/TGF beta 2/smad axis may be a potential target for OS treatment.
摘要：
Mounting evidence suggests that microRNAs (miRNAs) play important roles in the development of cancer by targeting expression of tumor-related genes. In the present study, downregulation of miR-193b was observed in hepatocellular carcinoma (HCC) tissues and HCC cell lines by quantitative RT-PCR analyses, suggesting that miR-193b is a tumor-suppressor in HCC. More importantly, miR-193b significantly enhanced the cytotoxicity of cisplatin in HepG2 cells by targeting Mc1-1. Knockdown of the Mc1-1 gene by specific siRNA exhibited a function similar to miR-193b on sensitizing HepG2 cells to cisplatin-inducing cytotoxicity. Furthermore, the miR-193b-induced sensitization of HepG2 cells to cisplatin cytotoxicity was abolished by the transfection of Mc-1 expression plasmid that lacked the 3'-untranslated region (3'-UTR). In addition, activation of caspase-3 was needed for sensitization by miR-193b to cisplatin-mediated cell death. Thus, the present study revealed the downregulation of miR-193b in HCC cells and illustrated a synergistic effect on cisplatin-induced apoptosis by targeting Mcl-1.
