Article
Biochemistry & Molecular Biology
Hee-Young Jeon, Majid Pornour, Hyunju Ryu, Sudeep Khadka, Rui Xu, Jihyun Jang, Deqiang Li, Hegang Chen, Arif Hussain, Ladan Fazli, Martin Gleave, Xuesen Dong, Furong Huang, Qianben Wang, Christopher Barbieri, Jianfei Qi
Summary: Overexpression of androgen receptor (AR) is the primary cause of castration-resistant prostate cancer, and this study reveals that SMAD3 plays a crucial role in upregulating AR expression by binding to intron 3 of the AR gene. Targeting SMAD3 binding sites can reduce AR levels and inhibit AR target gene expression. SMAD3 may also cooperate with or co-activate AR for AR target expression. These findings suggest that SMAD3 could be a potential target for inhibiting AR in prostate cancer.
NUCLEIC ACIDS RESEARCH
(2023)
Article
Medicine, Research & Experimental
Zhanjun Chen, Leyang Xiang, Longhai Li, Huohui Ou, Yinghao Fang, Yuyan Xu, Qin Liu, Zhigang Hu, Yu Huang, Xianghong Li, Dinghua Yang
Summary: The study revealed that linc00261 suppressed EMT and stem-like traits in HCC cells by inhibiting TGF-beta1/SMAD3 signaling.
JOURNAL OF TRANSLATIONAL MEDICINE
(2022)
Article
Cell Biology
Jun Zhou, Yasamin Dabiri, Rodrigo A. Gama-Brambila, Shahrouz Ghafoory, Mukaddes Altinbay, Arianeb Mehrabi, Mohammad Golriz, Biljana Blagojevic, Stefanie Reuter, Kang Han, Anna Seidel, Ivan Dikic, Stefan Wolfl, Xinlai Cheng
Summary: The study identifies pVHL as an E3 ligase for SMAD3 ubiquitination, which interacts with SMAD3 triggering its degradation, negatively regulating the TGF-beta/SMAD3 signaling pathway. Loss of pVHL in Drosophila leads to up-regulation of TGF-beta targets and a downward wing blade phenotype, rescued by inhibition of SMAD activity. The ectopic veinlets and reduced wing growth observed in Drosophila upon pVHL expression mirrors the effects seen with loss of TGF-beta/SMAD signaling.
JOURNAL OF CELL BIOLOGY
(2021)
Article
Immunology
Sonia Kiran, Mousumi Mandal, Ahmed Rakib, Amandeep Bajwa, Udai P. Singh
Summary: This study investigates the role and mechanism of miR-10a-3p in adipose inflammation and adipogenesis using ex vivo and in vitro approaches. The findings suggest that miR-10a-3p mimic reduces the expression of inflammatory cells and cytokines, and induces the expression of FoxP3 in adipose tissue. In vitro experiments also show that miR-10a-3p mimic reduces the expression of inflammatory genes and lipid accumulation. This study provides a new opportunity for the development of miR-10a-3p as a novel therapeutic for adipose inflammation and its associated metabolic disorders.
FRONTIERS IN IMMUNOLOGY
(2023)
Article
Oncology
Jinlu Ma, Mengjiao Cai, Yaqi Mo, Joshua S. Fried, Xinyue Tan, Yuan Ma, Jie Chen, Suxia Han, Bo Xu
Summary: Prostate cancer is a leading cause of cancer-related deaths in men, and mutations in the SPOP gene have been linked to clinical stage and metastasis of the disease. The interaction between SPOP and ITCH plays a key role in prostate cancer metastasis, with SPOP mutations disrupting this interaction and leading to increased levels of ITCH protein and higher cell invasion potential.
FRONTIERS IN ONCOLOGY
(2021)
Article
Oncology
Yuxuan Li, Pan Wang, Dongmei Ye, Xue Bai, Xuemei Zeng, Qiang Zhao, Zhiwei Zhang
Summary: This study investigated the expression of IGHG1 in gastric cancer and its effects on the proliferation, migration, invasion, and EMT of gastric cancer SGC7901 cells. High expression of IGHG1 was found in gastric cancer tissues, promoting cell proliferation, migration, and invasion. Low expression of IGHG1 reduced EMT-related protein expression and induced EMT in SGC7901 cells through the TGF-beta/SMAD3 signaling pathway.
Article
Pharmacology & Pharmacy
Ying Wang, Zhi Wang, Huiping Yang, Shuze Chen, Dekai Zheng, Xiuying Liu, Qinrui Jiang, Ye Chen
Summary: This study demonstrates the significant improvement of metformin on chronic colitis-related intestinal fibrosis, and reveals its possible mechanism. Metformin attenuates intestinal fibrosis by suppressing Smad3 phosphorylation and inhibiting fibroblast activation, proliferation, and collagen production.
FRONTIERS IN PHARMACOLOGY
(2022)
Review
Cell Biology
Maoduo Zhang, Ying Yi Zhang, Yongze Chen, Jia Wang, Qiang Wang, Hezhe Lu
Summary: The TGF-beta pathway in cancer has dual roles and is considered a potential new avenue for cancer therapy, but its functions and mechanisms of action require further investigation.
FRONTIERS IN CELL AND DEVELOPMENTAL BIOLOGY
(2021)
Article
Oncology
Shasha Liu, Chaoqi Zhang, Boqiao Wang, Huanyu Zhang, Guohui Qin, Congcong Li, Ling Cao, Qun Gao, Yu Ping, Kai Zhang, Jingyao Lian, Qitai Zhao, Dan Wang, Zhen Zhang, Xuan Zhao, Li Yang, Lan Huang, Bo Yang, Yi Zhang
Summary: The intense infiltration of regulatory T cells (Tregs) facilitates the qualities of glioma stem cells (GSCs) through TGF-beta secretion and NF-κB-IL6-STAT3 signaling pathway, leading to increased cancer stemness and tumorigenic potential. Blocking the IL6 receptor can mitigate the promotion effect of Tregs on glioma growth, and the expression levels of CD133, IL6, and TGF-beta could serve as prognosis markers for glioma patients.
CANCER IMMUNOLOGY IMMUNOTHERAPY
(2021)
Article
Oncology
Lian-Jing Cao, Yi-Jun Zhang, Si-Qi Dong, Xi-Zhao Li, Xia-Ting Tong, Dong Chen, Zi-Yi Wu, Xiao-Hui Zheng, Wen-Qiong Xue, Wei-Hua Jia, Jiang-Bo Zhang
Summary: The study found that elevated ATAD2 expression was significantly associated with lymph node metastasis, advanced clinical stage, and poor survival of ESCC patients. ATAD2 promotes ESCC metastasis through regulating the C/EBP beta /TGF-beta 1/Smad3/Snail signaling pathway.
JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
(2021)
Article
Biochemistry & Molecular Biology
Naohiro Nakamura, Katsunori Yoshida, Rinako Tsuda, Miki Murata, Takashi Yamaguchi, Kanehiko Suwa, Mayuko Ichimura, Koichi Tsuneyama, Koichi Matsuzaki, Toshiaki Nakano, Junko Hirohara, Toshihito Seki, Kazuichi Okazaki, M. Eric Gershwin, Makoto Naganuma
Summary: Patients with primary biliary cholangitis (PBC) are at higher risk for developing hepatocellular carcinoma (HCC), especially in the presence of comorbidities like excessive alcohol consumption. This study found that the balance of Smad signals may serve as a biomarker to predict the likelihood of HCC occurrence in PBC patients. Shifting favorably Smad phospho-isoforms through therapies could potentially reduce the risk of PBC-related HCC development.
FRONTIERS IN BIOSCIENCE-LANDMARK
(2021)
Article
Oncology
Zhe Tang, Patrick G. Pilie, Chuandong Geng, Ganiraju C. Manyam, Guang Yang, Sanghee Park, Daoqi Wang, Shan Peng, Cheng Wu, Guang Peng, Timothy A. Yap, Paul G. Corn, Bradley M. Broom, Timothy C. Thompson
Summary: ATR inhibitors in prostate cancer can activate immune pathways and induce cell autophagy, and when combined with anti-PD-L1 therapy, can result in a synergistic effect, providing therapeutic responses for CRPC patients.
CLINICAL CANCER RESEARCH
(2021)
Article
Biochemistry & Molecular Biology
Francesco Cambuli, Veronica Foletto, Alessandro Alaimo, Dario De Felice, Francesco Gandolfi, Maria Dilia Palumbieri, Michela Zaffagni, Sacha Genovesi, Marco Lorenzoni, Martina Celotti, Emiliana Bertossio, Giosue Mazzero, Arianna Bertossi, Alessandra Bisio, Francesco Berardinelli, Antonio Antoccia, Marco Gaspari, Mattia Barbareschi, Michelangelo Fiorentino, Michael M. Shen, Massimo Loda, Alessandro Romanel, Andrea Lunardi
Summary: This study demonstrates that non-canonical Activin A signaling plays a critical role in maintaining epithelial quiescence in the healthy prostate, with potential implications for understanding cancer initiation and the development of therapies targeting quiescent tumor progenitors.
Article
Cell Biology
Yu-Ting Huang, An-Chieh Cheng, Hui-Chi Tang, Guo-Cheng Huang, Ling Cai, Ta-Hsien Lin, Kou-Juey Wu, Ping-Hui Tseng, Greg G. Wang, Wei-Yi Chen
Summary: The study reveals that USP7 regulates the autoregulation of SMAD3 in p53-deficient lung cancer, inhibiting cell progression. USP7 mediates SMAD3 de-monoubiquitination, enhancing SMAD3 autoregulation to suppress cancer progression in p53-deficient lung cancer.
CELL DEATH & DISEASE
(2021)
Article
Biochemistry & Molecular Biology
Ruonan Bi, Yiqun Sun, Lili Xiang, Zhenzhen Xu, Xiaoyuan Ye, Yanying Tian, Yao Lin, Chunyan Yang, Yuguang Gao
Summary: Excessive fluoride intake during enamel development leads to dental fluorosis by affecting enamel mineralization. This study investigated the impact of fluoride on the expressions of RUNX2 and ALPL during mineralization and the effect of TGF-ss1 administration on fluoride treatment. The results indicated that fluoride exposure down-regulated RUNX2 and ALPL expression and decreased mineralization level. However, exogenous TGF-ss1 up-regulated RUNX2 and ALPL and promoted mineralization, mitigating the fluoride-induced suppression of ameloblast mineralization.
BIOLOGICAL TRACE ELEMENT RESEARCH
(2023)