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Your search keyword '"Hu, Chun"' showing total 3,397 results
Start Over Author "Hu, Chun" Publication Type Academic Journals
3,397 results on '"Hu, Chun"'

1. Exosomal miRNA 16-5p/29a-3p from pancreatic cancer induce adipose atrophy by inhibiting adipogenesis and promoting lipolysis.

Author

Tien, Sui-Chih, Chang, Chin-Chun, Huang, Ching-Hsuan, Peng, Hsuan-Yu, Chang, Yu-Ting, Chang, Ming-Chu, Lee, Wen-Hwa, and Hu, Chun-Mei

Subjects
Cell biology, Functional aspects of cell biology, Molecular physiology, Pathophysiology, Physiology
Abstract

Over 80% of the patients with pancreatic ductal adenocarcinoma (PDAC) have cachexia/wasting syndrome. Cachexia is associated with reduced survival, decreased quality of life, and higher metastasis rates. Here, we demonstrate that fat loss is the earliest feature of PDAC-exosome-induced cachexia. MicroRNA sequencing of exosomal components from normal and cancer-derived exosomes revealed enrichment of miR-16-5p, miR-21-5p, miR-29a-3p, and miR-125b-5p in serum exosomes of mice harboring PDAC and patients with PDAC. Further, miR-16-5p and miR-29a-3p inhibited adipogenesis through decreasing Erlin2 and Cmpk1 expression which downregulates C/EBPβ and PPARγ. Synergistically, miR-29a-3p promotes lipolysis through increasing ATGL expression by suppressing MCT1 expression. Furthermore, PDAC-exosomes deprived of miR-16-5p and miR-29a-3p fail to induce fat loss. Hence, miR-16-5p and miR-29a-3p exosomal miRs are essential for PDAC-induced fat loss. Thus, we unravel that PDAC induces adipose atrophy via exosomal miRs. This knowledge may provide new diagnostic and therapeutic strategies for PDAC-induced cachexia.

Published
2024

5. Unraveling the impact of cancer-associated fibroblasts on hypovascular pancreatic neuroendocrine tumors

Author

Lai, Ting-Yu, Chiang, Tsai-Chen, Lee, Chih-Yuan, Kuo, Ting-Chun, Wu, Chien-Hui, Chen, Yi-Ing, Hu, Chun-Mei, Maskey, Manjit, Tang, Shiue-Cheng, Jeng, Yung-Ming, Tien, Yu-Wen, Lee, Eva Y-HP, and Lee, Wen-Hwa

Subjects
Biomedical and Clinical Sciences, Oncology and Carcinogenesis, Digestive Diseases, Cancer, Rare Diseases, Aetiology, 2.1 Biological and endogenous factors, Public Health and Health Services, Oncology & Carcinogenesis, Oncology and carcinogenesis
Abstract

BackgroundPancreatic neuroendocrine tumors (PNETs) with low microvessel density and fibrosis often exhibit clinical aggressiveness. Given the contribution of cancer-associated fibroblasts (CAFs) to the hypovascular fibrotic stroma in pancreatic ductal adenocarcinoma, investigating whether CAFs play a similar role in PNETs becomes imperative. In this study, we investigated the involvement of CAFs in PNETs and their effects on clinical outcomes.MethodsWe examined 79 clinical PNET specimens to evaluate the number and spatial distribution of α-smooth muscle actin (SMA)-positive cells, which are indicative of CAFs. Then, the findings were correlated with clinical outcomes. In vitro and in vivo experiments were conducted to assess the effects of CAFs (isolated from clinical specimens) on PNET metastasis and growth. Additionally, the role of the stromal-cell-derived factor 1 (SDF1)-AGR2 axis in mediating communication between CAFs and PNET cells was investigated.ResultsαSMA-positive and platelet-derived growth factor-α-positive CAFs were detected in the hypovascular stroma of PNET specimens. A higher abundance of α-SMA-positive CAFs within the PNET stroma was significantly associated with a higher level of clinical aggressiveness. Notably, conditioned medium from PNET cells induced an inflammatory phenotype in isolated CAFs. These CAFs promoted PNET growth and metastasis. Mechanistically, PNET cells secreted interleukin-1, which induced the secretion of SDF1 from CAFs. This cascade subsequently elevated AGR2 expression in PNETs, thereby promoting tumor growth and metastasis. The downregulation of AGR2 in PNET cells effectively suppressed the CAF-mediated promotion of PNET growth and metastasis.ConclusionCAFs drive the growth and metastasis of aggressive PNETs. The CXCR4-SDF1 axis may be a target for antistromal therapy in the treatment of PNET. This study clarifies mechanisms underlying PNET aggressiveness and may guide future therapeutic interventions targeting the tumor microenvironment.

Published
2024

7. Association between pretreatment emotional distress and immune checkpoint inhibitor response in non-small-cell lung cancer

Author

Zeng, Yue, Hu, Chun-Hong, Li, Yi-Zheng, Zhou, Jian-Song, Wang, Shu-Xing, Liu, Meng-Dong, Qiu, Zhen-Hua, Deng, Chao, Ma, Fang, Xia, Chun-Fang, Liang, Fei, Peng, Yu-Rong, Liang, Ao-Xi, Shi, Sheng-Hao, Yao, Shi-Jiao, Liu, Jun-Qi, Xiao, Wen-Jie, Lin, Xiao-Qiao, Tian, Xin-Yu, Zhang, Ying-Zhe, Tian, Zhuo-Ying, Zou, Ji-An, Li, Yun-Shu, Xiao, Chao-Yue, Xu, Tian, Zhang, Xiao-Jie, Wang, Xiao-Ping, Liu, Xian-Ling, and Wu, Fang

Published
2024
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9. Oncogenic KRAS, Mucin 4, and Activin A‐Mediated Fibroblast Activation Cooperate for PanIN Initiation

Author

Hu, Chun‐Mei, Huang, Chien‐Chang, Hsu, Min‐Fen, Chien, Hung‐Jen, Wu, Pei‐Jung, Chen, Yi‐Ing, Jeng, Yung‐Ming, Tang, Shiue‐Cheng, Chung, Mei‐Hsin, Shen, Chia‐Ning, Chang, Ming‐Chu, Chang, Yu‐Ting, Tien, Yu‐Wen, and Lee, Wen‐Hwa

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Cancer, Genetics, Digestive Diseases, Pancreatic Cancer, Prevention, Rare Diseases, Aetiology, 2.1 Biological and endogenous factors, Mice, Humans, Animals, Proto-Oncogene Proteins p21(ras), Mucin-4, Pancreatic Neoplasms, Carcinoma, Pancreatic Ductal, Mice, Transgenic, Carcinoma in Situ, alpha SMA(+) fibroblast, activin A, PanIN, Kras, Muc4, αSMA+ fibroblast
Abstract

Over 90% of patients with pancreatic ductal adenocarcinoma (PDAC) have oncogenic KRAS mutations. Nevertheless, mutated KRAS alone is insufficient to initiate pancreatic intraepithelial neoplasia (PanIN), the precursor of PDAC. The identities of the other factors/events required to drive PanIN formation remain elusive. Here, optic-clear 3D histology is used to analyze entire pancreases of 2-week-old Pdx1-Cre; LSL-KrasG12D/+ (KC) mice to detect the earliest emergence of PanIN and observed that the occurrence is independent of physical location. Instead, it is found that the earliest PanINs overexpress Muc4 and associate with αSMA+ fibroblasts in both transgenic mice and human specimens. Mechanistically, KrasG12D/+ pancreatic cells upregulate Muc4 through genetic alterations to increase proliferation and fibroblast recruitments via Activin A secretion and consequently enhance cell transformation for PanIN formation. Inhibition of Activin A signaling using Follistatin (FST) diminishes early PanIN-associated fibroblast recruitment, effectively curtailing PanIN initiation and growth in KC mice. These findings emphasize the vital role of interactions between oncogenic KrasG12D/+ -driven genetic alterations and induced microenvironmental changes in PanIN initiation, suggesting potential avenues for early PDAC diagnostic and management approaches.

Published
2023

17. De novo GRIN variants in M3 helix associated with neurological disorders control channel gating of NMDA receptor

Author

Xu, Yuchen, Song, Rui, Perszyk, Riley E., Chen, Wenjuan, Kim, Sukhan, Park, Kristen L., Allen, James P., Nocilla, Kelsey A., Zhang, Jing, XiangWei, Wenshu, Tankovic, Anel, McDaniels, Ellington D., Sheikh, Rehan, Mizu, Ruth K., Karamchandani, Manish M., Hu, Chun, Kusumoto, Hirofumi, Pecha, Joseph, Cappuccio, Gerarda, Gaitanis, John, Sullivan, Jennifer, Shashi, Vandana, Petrovski, Slave, Jauss, Robin-Tobias, Lee, Hyun Kyung, Bozarth, Xiuhua, Lynch, David R., Helbig, Ingo, Pierson, Tyler Mark, Boerkoel, Cornelius F., Myers, Scott J., Lemke, Johannes R., Benke, Timothy A., Yuan, Hongjie, and Traynelis, Stephen F.

Published
2024
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28. The Role of Folate Deficiency as a Potential Risk Factor for Nontraumatic Anterior Spinal Artery Syndrome in an Adolescent Girl.

Author

Hu, Chun-Chieh, Yang, Yung-Yu, Luxton, G, Lin, Yu-Pang, Hung, Kuo-Sheng, and Hu, Chih-Fen

Subjects
acute flaccid paralysis, folate deficiency, nontraumatic anterior spinal artery syndrome, young stroke
Abstract

Nontraumatic anterior spinal artery syndrome (ASAS) is an extremely rare clinical condition in pediatric populations with a mostly unknown underlying etiology. Here we discuss the case of a previously healthy 14-year-old girl presenting with sudden onset acute flaccid paralysis to the emergency department. A spinal STIR/DWI MRI revealed hyperintensities extending from cervical vertebrae C3-6, consistent with the diagnosis of ASAS. In order to determine any precipitating causes of ASAS, we also extensively investigated established potential risk factors for ASAS in our patient and noticed that she had a marked folate deficiency requiring folic acid supplementation to prevent future episodes of ASAS as well as to repair the patients injured spinal cord. Interestingly, the patient did not display elevated levels of homocysteine nor did she possess the three pathogenic MTHFR mutations characteristic of ASAS. Although her folate deficiency did not cause responsive hyperhomocysteinemia, and she did not have pathogenic MTHFR mutations that impair the function of methylenetetrahydrofolate reductase in folate cycle, we suggest that isolated folate deficiency may play a role in adolescent cases of ASAS that, once identified, would require prompt identification and early intervention to improve the prognosis of these patients.

Published
2022

29. Structural basis of interleukin-17B receptor in complex with a neutralizing antibody for guiding humanization and affinity maturation

Author

Lee, Wen-Hsin, Chen, Xiaorui, Liu, I-Ju, Lee, Jiin-Horng, Hu, Chun-Mei, Wu, Han-Chung, Wang, Sheng-Kai, Lee, Wen-Hwa, and Ma, Che

Subjects
Biochemistry and Cell Biology, Biological Sciences, Immunization, Biotechnology, Cancer, Digestive Diseases, Aetiology, 2.1 Biological and endogenous factors, Humans, Mice, Animals, Receptors, Interleukin-17, Interleukin-17, Fibronectins, Ligands, Antibodies, Neutralizing, Gene Expression Regulation, Neoplastic, Carcinogenesis, Antibodies, Monoclonal, CP: Cancer, CP: Immunology, X-ray crystal structure, antibody, antibody affinity maturation, complex structure, humanized antibody, interleukin-17 receptor B, IL-17RB, pancreatic cancer, targeting therapy, Medical Physiology, Biological sciences
Abstract

Upregulation of interleukin-17 receptor B (IL-17RB) is known to be oncogenic, while other IL-17 receptors and ligands are generally involved in pro-inflammatory pathways. We identify a mouse neutralizing monoclonal antibody (mAb) D9, which blocks the IL-17RB/IL-17B pathway and inhibits pancreatic tumorigenesis in an orthotopic mouse model. The X-ray crystal structure of the IL-17RB ectodomain in complex with its neutralizing antibody D9 shows that D9 binds to a predicted ligand binding interface and engages with the A'-A loop of IL-17RB fibronectin III domain 1 in a unique conformational state. This structure also provides important paratope information to guide the design of antibody humanization and affinity maturation of D9, resulting in a humanized 1B12 antibody with marginal affinity loss and effective neutralization of IL-17B/IL-17RB signaling to impede tumorigenesis in a mouse xenograft model.

Published
2022

50. AIWW: a new nutrition-screening tool for the oncologic population

Author

Ge, Yi-Zhong, Fu, Zhen-Ming, Zhang, Qi, Song, Meng-Meng, Ruan, Guo-Tian, Zhang, Xi, Zhang, Xiao-Wei, Li, Xiang-Rui, Zhang, Kang-Ping, Tang, Meng, Liu, Xiao-Yue, Yang, Ming, Liu, Tong, Xie, Hai-Lun, Zhang, He-Yang, Wang, Zi-Wen, Hu, Chun-Lei, Lin, Shi-Qi, Zhang, Rui, Xu, Hong-Xia, Li, Wei, Song, Chun-Hua, Liu, Ming, Chen, Jun-Qiang, Wang, Kun-Hua, Bo, Li, Cong, Ming-Hua, Li, Zeng-Ning, Guo, Zeng-Qin, Wang, Xiao-Bin, Wang, Bin-Yan, Xu, Benjamin, Qin, Xian-Hui, Xu, Xi-Ping, Barazzoni, Rocco, Yao, Qing-Hua, Weng, Min, Shen, Xian, and Shi, Han-Ping

Published
2023
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