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8. Mfsd2a suppresses colorectal cancer progression and liver metastasis via the S100A14/STAT3 axis.

Author

Sun, Linfeng, Li, Xiangdong, Xiao, Yuhao, Yu, Wenjie, Chen, Xuyang, Wang, Ziyi, Xia, Nan, Chen, Xuejiao, Chen, Minhao, Zhu, Haoliang, Li, Jie, Wei, Jie, Han, Sheng, and Pu, Liyong

Subjects
COLORECTAL liver metastasis, LIVER metastasis, MEDICAL sciences, MASS spectrometry, STOMACH cancer
Abstract

Background: Colorectal cancer (CRC) exhibits a high incidence globally, with the liver being the most common site of distant metastasis. At the time of diagnosis, 20–30% of CRC patients already present with liver metastases. Colorectal liver metastasis (CRLM) is a major cause of mortality among CRC patients. The pathogenesis of CRLM involves complex molecular mechanisms and the hepatic immune microenvironment, but current clinical prevention and treatment are significantly limited. Recent studies have revealed that the major facilitator superfamily domain containing protein-2a (Mfsd2a) plays a pivotal role in the development and metastasis of various cancers. For instance, Mfsd2a inhibits gastric cancer initiation and progression and may impact angiogenesis. However, the mechanisms by which Mfsd2a influences CRC progression and liver metastasis remain unclear. Methods: In this study, we conducted a survival analysis of Mfsd2a in colorectal cancer using data from the GEPIA and GEO databases, and examined the expression differences between primary tumor (PT) and liver metastasis (LM). We further assessed the clinical significance and prognostic relevance of Mfsd2a through immunohistochemical analysis of tissue samples from 70 CRLM patients. Moreover, Kaplan-Meier analysis was used to perform survival analysis on these patients. The biological function of Mfsd2a in CRLM was confirmed by a series of experiments conducted both in vitro and in vivo. Additionally, we investigated downstream molecular pathways using western blot, Co-immunoprecipitation, immunofluorescence, and mass spectrometry techniques. Results: We observed that Mfsd2a expression is reduced in LM compared to PT, and higher Mfsd2a levels are associated with better prognosis in CRLM patients. Furthermore, function assays demonstrated that Mfsd2a suppresses CRC cells proliferation, migration, invasion, and EMT in vitro, while also delaying tumor growth and liver metastasis in vivo. Mechanistically, Mfsd2a interacts with S100A14, enhancing its expression and inhibiting phosphorylation of STAT3. In addition, the STAT3 activator colivelin partially reversed the inhibitory effect of Mfsd2a overexpression on the progression of colorectal cancer and liver metastasis. Conclusion: In summary, Mfsd2a inhibits colorectal cancer progression and liver metastasis by interacting with S100A14, thereby suppressing the phosphorylation of STAT3. Mfsd2a functions as a tumor suppressor in CRLM and could be a promising therapeutic target for treating CRC patients with liver metastasis. [ABSTRACT FROM AUTHOR]

Published
2025
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13. Endothelial DGKG promotes tumor angiogenesis and immune evasion in hepatocellular carcinoma

Author

Zhang, Liren, primary, Xu, Jiali, additional, Zhou, Suiqing, additional, Yao, Feifan, additional, Zhang, Ruizhi, additional, You, Wenhua, additional, Yu, Kai, additional, Zhang, Yu, additional, Baheti, Tasiken, additional, Pu, Liyong, additional, Xu, Jing, additional, Qian, Xiaofeng, additional, Xia, Yongxiang, additional, Dai, Xinzheng, additional, Li, Qing, additional, and Wang, Xuehao, additional

Published
2023
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15. Hepatocyte SGK1 activated by hepatic ischemia-reperfusion promotes the recurrence of liver metastasis via IL-6/STAT3

Author

Li, Xiangdong, primary, Wang, Ziyi, additional, Jiao, Chenyu, additional, Zhang, Yu, additional, Xia, Nan, additional, Yu, Wenjie, additional, Chen, Xuejiao, additional, Wikana, Likalamu Pascalia, additional, Liu, Yue, additional, Sun, Linfeng, additional, Chen, Minhao, additional, Xiao, Yuhao, additional, Shi, Yuhua, additional, Han, Sheng, additional, and Pu, Liyong, additional

Published
2022
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16. Targeting hepatocyte MagL regulates the progression of colorectal liver metastases during liver ischemia-reperfusion

Author

Xia, Nan, primary, Wang, Ziyi, additional, Liu, Yue, additional, Li, Xiangdong, additional, Zhang, Yu, additional, Yu, Wenjie, additional, Likalamu, Pascalia Wikana, additional, Chen, Minhao, additional, Xiao, Yuhao, additional, Sun, Linfeng, additional, Han, Sheng, additional, Shi, Yuhua, additional, and Pu, Liyong, additional

Published
2022
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17. Myeloid Trem2 orchestrates nonalcoholic steatohepatitis-associated inflammation and HCC progression by reprogramming recruited macrophages

Author

Wang, Xuehao, primary, Wang, Ziyi, additional, Zhang, Yu, additional, Han, Sheng, additional, Li, Xiangdong, additional, Nie, Huiling, additional, Jiao, Chenyu, additional, Xia, Nan, additional, Yu, Wenjie, additional, Chen, Minhao, additional, Wang, Hao, additional, Chen, Xuejiao, additional, Chen, Xiaoyuan, additional, and Pu, Liyong, additional

Published
2022
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24. Efficacy and safety of camrelizumab plus apatinib during the perioperative period in resectable hepatocellular carcinoma: a single-arm, open label, phase II clinical trial

Author

Xia, Yongxiang, primary, Tang, Weiwei, additional, Qian, Xiaofeng, additional, Li, Xiangcheng, additional, Cheng, Feng, additional, Wang, Ke, additional, Zhang, Feng, additional, Zhang, Chuanyong, additional, Li, Donghua, additional, Song, Jinhua, additional, Zhang, Hui, additional, Zhao, Jie, additional, Yao, Aihua, additional, Wu, Xiaofeng, additional, Wu, Chen, additional, Ji, Guwei, additional, Liu, Xisheng, additional, Zhu, Feipeng, additional, Qin, Lang, additional, Xiao, Xuan, additional, Deng, Zhenhua, additional, Kong, Xiangyi, additional, Li, Si, additional, Yu, Yangyang, additional, Xi, Wenjing, additional, Deng, Wanglong, additional, Qi, Chuang, additional, Liu, Hanyuan, additional, Pu, Liyong, additional, Wang, Ping, additional, and Wang, Xuehao, additional

Published
2022
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30. Preliminary efficacy and safety of perioperative treatment of camrelizumab combined with apatinib in resectable hepatocellular carcinoma (HCC): A prospective phase II study.

Author

Xia, Yongxiang, primary, Wang, Ping, additional, Pu, Liyong, additional, Qian, Xiaofeng, additional, Cheng, Feng, additional, Wang, Ke, additional, Zhang, Chuanyong, additional, Li, Donghua, additional, Li, Xiangcheng, additional, Zhang, Feng, additional, Zhao, Jie, additional, Li, Si, additional, Xi, Wenjing, additional, and Wang, Xuehao, additional

Published
2021
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37. Hypomethylation‐mediated activation of cancer/testis antigen KK‐LC‐1 facilitates hepatocellular carcinoma progression through activating the Notch1/Hes1 signalling

Author

Chen, Zhiqiang, primary, Zuo, Xueliang, additional, Pu, Liyong, additional, Zhang, Yao, additional, Han, Guoyong, additional, Zhang, Long, additional, Wu, Zhengshan, additional, You, Wei, additional, Qin, Jianjie, additional, Dai, Xinzheng, additional, Shen, Hongbing, additional, Wang, Xuehao, additional, and Wu, Jindao, additional

Published
2019
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38. 5‐Hydroxytryptamine Receptor 1D Aggravates Hepatocellular Carcinoma Progression Through FoxO6 in AKT‐Dependent and Independent Manners

Author

Zuo, Xueliang, primary, Chen, Zhiqiang, additional, Cai, Juan, additional, Gao, Wen, additional, Zhang, Yao, additional, Han, Guoyong, additional, Pu, Liyong, additional, Wu, Zhengshan, additional, You, Wei, additional, Qin, Jianjie, additional, Dai, Xinzheng, additional, Shen, Hongbing, additional, Wu, Jindao, additional, and Wang, Xuehao, additional

Published
2019
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49. Correction: miR-146a Ameliorates Liver Ischemia/Reperfusion Injury by Suppressing IRAK1 and TRAF6.

Author

Jiang, Weiwei, Kong, Liangliang, Ni, Qingfeng, Lu, Yeting, Ding, Wenzhou, Liu, Guoqing, Pu, Liyong, Tang, Weibing, and Kong, Lianbao

Subjects
REPERFUSION injury, REPERFUSION, ISCHEMIA, IMMUNOSTAINING, LIVER
Abstract

The corresponding author explained that 10 mice were used in each group whilst performing liver ischemia/reperfusion experiments, but that two liver samples of the Ago-mir-NC group were damaged during embedding or sectioning, and as a result this group only contained 8 samples. Specifically, the Fig 6D Ago-mir-146a panel appeared similar to the Fig 6G Ago-mir-146a panel despite being used to represent different experimental conditions. They provided an updated Fig 6 with the correct Fig 6D Ago-mir-146a image obtained in the original experiment, as well as the individual level data underlying the published results (S1 File). [Extracted from the article]

Published
2023
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50. circLARP4 induces cellular senescence through regulating miR‐761/RUNX3/p53/p21 signaling in hepatocellular carcinoma.

Author

Chen, Zhiqiang, Zuo, Xueliang, Pu, Liyong, Zhang, Yao, Han, Guoyong, Zhang, Long, Wu, Jindao, and Wang, Xuehao

Abstract

Circular RNAs (circRNAs), a novel class of non‐coding RNAs, have emerged as indispensable modulators in human malignancies. Aberrant cellular senescence is a phenotype observed in various cancers. The association of circRNAs with cellular senescence in tumors is yet to determined. Here, we investigated the role of circLARP4 in cellular senescence and cell proliferation in hepatocellular carcinoma (HCC). Downregulated circLARP4 level was observed in HCC tissues and cell lines. Low expression level of circLARP4 independently predicted poor survival outcome. Gain‐of‐function and loss‐of‐function assays demonstrated that circLARP4 suppressed HCC cell proliferation, mediated cell cycle arrest and induced senescence in vitro. Levels of p53 and p21, 2 key regulatory molecules in cellular senescence, were increased in circLARP4‐overexpressed HCC cells and decreased in circLARP4‐silenced HCC cells. In vivo experiments further confirmed the tumor‐suppressing activity of circLARP4. Further mechanistic studies showed that circLARP4 dampened HCC progression by sponging miR‐761, thereby promoting the expression level of RUNX3 and activating the downstream p53/p21 signaling. Our study revealed the role of circLARP4/miR‐761/RUNX3/p53/p21 signaling in HCC progression, providing a potential survival predictor and therapeutic candidate for HCC. circLARP4 is downregulated in hepatocellular carcinoma. circLARP4 suppresses hepatocellular carcinoma cell proliferation, mediates cell cycle arrest and induces senescence. circLARP4 dampens hepatocellular carcinoma progression by sponging miR‐761, thereby promoting the expression of RUNX3 and activating the downstream p53/p21 signaling. [ABSTRACT FROM AUTHOR]

Published
2019
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