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| 1 | Circulating lung cancer tumor cells isolated by the EpCAM-independent enrichment strategy correlate with Cytokeratin 19-derived CYFRA21-1 and pathological staging显示文摘 | Qian Chen Feng Ge Wei Cui Fei Wang Zhuo Yang Ye Guo Longyun Li Ross Macrae Bremner Peter Ping Lin | 2013 | Clinica Chimica Acta2013，，： | 1 |
| 2 | The effect of inorganic salt on the structure of filter cake of water based drilling fluid显示文摘 | YAO Rugang JIANG Guancheng YE Longyun | 2014 | Proceedings2014，，01： | 1 |
| 3 | LncRNA LIMT(LINC01089)contributes to sorafenib chemoresistance via regulation of miR-665 and epithelial to mesenchymal transition in hepatocellular carcinoma cells显示文摘Hepatocellular carcinoma(HCC)is one of the most malignant tumors worldwide and HCC patients often develop drug resisitene.Long non-coding RNAs(LncRNAs)are closely related to cell cycle,growth,development,differentiation,and apoptosis.Abnormally expressed lncRNAs have been proved to mediate drug resistance in tumor cells.However,the effect of LIMT on drug resistance has not been explored in HCC.In this study,we explored the effect of long non-coding RNA LIMT on drug resistance and its underlying mechanism in hepatocellular carcinoma(HCC).Our results showed that LncRNA LINC01089(LIMT)expression is downregulated in 78.57%(44/56)of 56 HCC tumor tissue samples.LIMT expression is also downregulated in HCC cells compared with that in normal liver LO2 cells.Inhibition of LIMT increases the resistance to sorafenib and promotes cell invasion via regulation of epithelial to mesenchymal transition(EMT)in HCC.StarBase V3.0 was used to predict the potential binding site of miR-665 in LIMT.Furthermore,miR-665 participates in sorafenib resistance and also regulates the level of EMT-related proteins in HCC cells.A rescue experiment demonstrated that silencing of LIMT eliminats the inhibitory effect of the miR-665 inhibitor on sorafenib resistance in HCC cells.Taken together,our findings revealed that downregulation of LIMT increases the resistance of HCC to sorafenib via miR-665 and EMT.Therefore,LIMT,which serves as a therapeutically effective target,will provide new hope for the treatment of HCC. | Jing Sun Xiaoxiao Zheng Baoming Wang Ying Cai Li Zheng Liqiang Hu Xuemei Lu Shangzhi Xie Xin Zhang Hao Liu Longyun Ye | 2022 | Acta Biochimica et Biophysica Sinica2022，54，2： | 1 |
| 4 | Novel strategy for oncogenic alteration-induced lipid metabolism reprogramming in pancreatic cancer显示文摘The pathogenesis of pancreatic cancer involves substantial metabolic reprogramming,resulting in abnormal proliferation of tumor cells.This tumorigenic reprogramming is often driven by genetic mutations,such as acti-vating mutations of the KRAS oncogene and inactivating or deletions of the tumor suppressor genes SMAD4,CDKN2A,and TP53,which play a critical role in the initiation and development of pancreatic cancer.As a normal cell gradually develops into a cancer cell,a series of signature characteristics are acquired:activation of signaling pathways that sustain proliferation;an ability to resist growth inhibitory signals and evade apoptosis;and an ability to generate new blood vessels and invade and metastasize.In addition to these features,recent research has revealed that metabolic reprogramming and immune escape are two other novel characteristics of tumor cells.The effect of the interactions between tumor and immune cells on metabolic reprogramming is a key factor determining the antitumor immunotherapy response.Lipid metabolism reprogramming,a feature of many malignancies,not only plays a role in maintaining tumor cell proliferation but also alters the tumor microenvironment by inducing the release of metabolites that in turn affect the metabolism of normal immune cells,ultimately leading to the at-tenuation of the antitumor immune response and resistance to immunotherapy.Pancreatic cancer has been found to have substantial lipid metabolism reprogramming,but the mechanisms remain elusive.Therefore,this review focuses on the mechanisms regulating lipid metabolism reprogramming in pancreatic cancer cells to provide new therapeutic targets and aid the development of new therapeutic strategies for pancreatic cancer. | Duancheng Guo Longyun Ye Weiding Wu Xianjun Yu Kaizhou Jin | 2023 | Acta Biochimica et Biophysica Sinica2023，55，6： | 0 |
| 5 | COM33 suppresses carboplatin-induced epithelial-mesenchymal transition via inhibition of Twist1 in ovarian cancer显示文摘Despite favorable responses to platinum-based chemotherapy in ovarian cancer(OC),chemoresistance is still a major cause of treatment failure.Hence,we develop a novel synthetic agent,COM33,to relieve the chemoresistance caused by carboplatin.The anti-cancerous effects of the combination of COM33 and carboplatin on OC are evaluated by cell viability,wound healing,and transwell invasion assays.A mechanistic investigation is carried out by using RNA-Seq analysis and then verified by western blot analysis and immunofluorescence microscopy.The safety and efficacy in vivo are evaluated using SKOV3 tumor-bearing nude mice.Results show that the co-administration of COM33 enhances the inhibitory effects of carboplatin on cancer cell viability,migration,and invasion in vitro and tumor growth in vivo.Furthermore,COM33 suppresses the carboplatin-induced epithelialmesenchymal transition(EMT)by inhibiting the ERK signaling pathway.Additionally,we show that Twist1,the effector of the ERK signaling pathway,participates in carboplatin-induced EMT and is also inhibited by COM33.Our data show that the combination of carboplatin with COM33 is beneficial for chemotherapy against OC,which may be a potential novel anti-tumor strategy. | Zhiyang Zhou Li Jin Jian Shen Weihui Shi Yue Xu Longyun Ye Junxi Liu Jiexue Pan | 2023 | Acta Biochimica et Biophysica Sinica2023，55，1： | 0 |
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