Article
Environmental Sciences
Shiwen Liu, Yumeng Hu, Yue Wang, Yeqing Sun, Shu-Lan Qin, Dan Xu
Summary: The study found that endosulfan may cause excessive cell proliferation and accumulation of extracellular matrix in human renal mesangial cells through the TGF-β/Smad signaling pathway, as well as induce oxidative stress and inflammation.
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
(2021)
Article
Oncology
Bei Pu, Xu Zhang, Tengfeng Yan, Yuntao Li, Baohui Liu, Zhihong Jian, Omer Kamal Mahgoub, Lijuan Gu, Xiaoxing Xiong, Ning Zou
Summary: Recent studies have shown that MICAL2 plays a role in promoting proliferation and migration of glioblastoma through the TGF-beta/p-Smad2/EMT-like signaling pathway. Knockdown of MICAL2 can inhibit the growth and invasion abilities of glioblastoma cells. High MICAL2 expression predicts poor prognosis in GBM patients, making it a potential therapeutic target.
FRONTIERS IN ONCOLOGY
(2021)
Article
Oncology
Yanyan Feng, Chuanyu Sun, Lifeng Zhang, Hongyuan Wan, Hangsheng Zhou, Yongquan Chen, Lijie Zhu, Guowei Xia, Yuanyuan Mi
Summary: The coatomer protein complex subunit beta 2 (COPB2) plays an important role in prostate cancer by promoting the proliferation and invasion of cancer cells through the regulation of the MAPK/TGF-beta signaling pathway. COPB2 could potentially serve as a new biomarker for diagnosis and monitoring of prostate cancer.
FRONTIERS IN ONCOLOGY
(2022)
Article
Immunology
Min Chao, Nan Liu, Zhichuan Sun, Yongli Jiang, Tongtong Jiang, Meng Xv, Lintao Jia, Yanyang Tu, Liang Wang
Summary: Sox9, an upregulated transcription factor in clinical gliomas associated with poor prognosis, promotes migration and invasion of glioma cells and in vivo tumor development. It functions downstream of the TGF-beta pathway, where TGF-beta signaling prevents proteasomal degradation of Sox9 protein in glioma cells. These findings provide new insights into the interaction between TGF-beta signaling and oncogenic transcription factors, with implications for targeted therapy and prognostic assessment of gliomas.
FRONTIERS IN IMMUNOLOGY
(2021)
Article
Biochemistry & Molecular Biology
Ryoko Nagano, Shinsuke Fujii, Kana Hasegawa, Hidefumi Maeda, Tamotsu Kiyoshima
Summary: Tooth germ development involves reciprocal interactions between odontogenic epithelium and adjacent mesenchyme. Wnt/f3-catenin signaling contributes to tooth germ development through YAP1-TGF-f3 signaling.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2022)
Article
Oncology
Justin Joseph, Capucine R. Magaut, Simon Storevik, Luiz H. Geraldo, Thomas Mathivet, Md Abdul Latif, Justine Rudewicz, Joris Guyon, Matteo Gambaretti, Frida Haukas, Amalie Trones, Lars A. Romo Ystaas, Jubayer A. Hossain, Sandra Ninzima, Sylvain Cuvellier, Wenjing Zhou, Tushar Tomar, Barbara Klink, Lalit Rane, Bronwyn K. Irving, Joanne Marrison, Peter O'Toole, Heiko Wurdak, Jian Wang, Zhang Di, Even Birkeland, Frode S. Berven, Frank Winkler, Frank A. E. Kruyt, Andreas Bikfalvi, Rolf Bjerkvig, Thomas Daubon, Hrvoje Miletic
Summary: Analysis of TCGA data revealed a high activation of the TGF-beta pathway in GBMs compared to oligodendroglial tumors. Stimulation of GBM cell lines with TGF-beta 1 enhanced MT formation and communication via calcium signaling, while inhibition of the TGF-beta pathway significantly reduced MT formation and invasion. Downstream of TGF-beta, thrombospondin 1 (TSP1) was identified as a potential mediator of MT formation in GBM, which was upregulated upon TGF-beta stimulation and inhibited MT formation when knocked down in vitro and in vivo.
Article
Pharmacology & Pharmacy
Wenfang Bao, Jialin Wang, Kailing Fan, Yong Gao, Jingde Chen
Summary: Ferroptosis, a distinct iron-dependent programmed cell death mechanism, has been suggested as a potential approach in cancer therapy. This study identified PIAS3 as a driver of ferroptosis in HCC and revealed the regulatory axis of PIAS3/TGF-beta/TXNIP, providing a potential avenue for employing ferroptosis in HCC treatment.
PHARMACOLOGICAL RESEARCH
(2023)
Article
Cell Biology
Xinyuan Liu, Jian Xu, Bingbing Shen, Jichuan Xu, Jianxin Jiang
Summary: Pancreatic cancer (PC) is the fourth leading cause of cancer-related death worldwide, with a survival rate below 5%. Abnormal proliferation and distant metastasis are major challenges for the diagnosis and treatment of PC, making it crucial for researchers to understand the molecular mechanisms underlying PC proliferation and metastasis. This study found that USP33, a member of the deubiquitinating enzyme family, is upregulated in PC samples and cells, and its high expression is associated with poor prognosis. Functional experiments showed that USP33 overexpression promotes PC cell proliferation, migration, and invasion, while inhibition of USP33 has the opposite effect. The study also identified TGFBR2 as a potential binding protein of USP33 and revealed a positive feedback loop between USP33 and the TGF-beta signaling pathway.
CELL DEATH & DISEASE
(2023)
Article
Pharmacology & Pharmacy
Qian Huang, Rui Xiao, Jing Lu, Yao Zhang, Liang Xu, Jie Gao, Jing Sun, Haiping Wang
Summary: This study revealed that endoglin exacerbated PF by regulating the activation of TGF-beta/ALK/Smads signaling, while its knockdown could alleviate peritoneal injury, providing a novel potential therapeutic target in PF.
FRONTIERS IN PHARMACOLOGY
(2022)
Article
Oncology
Changfu Liu, Weihao Zhang, Junfeng Wang, Tongguo Si, Wenge Xing
Summary: TAMs promote colorectal cancer progression by inducing glycolytic state, stem-like phenotypes, and invasion through HIF1 alpha/TRIB3-dependent activation of beta-catenin/Wnt signaling pathway. Blocking HIF1 alpha signals may improve chemotherapy outcomes in colorectal cancer treatment.
Article
Biochemistry & Molecular Biology
Ping Li, Yahao Zhao, Yongze Liu, Yuelei Zhao, Yunqin Yan, Shuang Li, Shufeng Li, Huili Tong
Summary: Cyanocobalamin (CNCbl) promotes the differentiation of C2C12 cells by upregulating the expression of Acvr1, p-Smad2, and p-Smad3 in the TGF-beta signaling pathway. Inhibition of CD320 reduces CNCbl uptake and downregulates the expression of differentiation marker proteins. Furthermore, injection of CNCbl accelerates mouse muscle injury repair.
Article
Oncology
Yun Wu, Ying Lin, Junfan Pan, Xunwei Tu, Yiquan Xu, Hongru Li, Yusheng Chen
Summary: This study identified NCAPG as a hub gene in lung adenocarcinoma (LUAD), with strong associations to clinical stage, M-classification, and N-classification. NCAPG was found to be a prognostic risk factor for LUAD, promoting proliferation and migration via the TGF-beta signaling pathway.
CANCER CELL INTERNATIONAL
(2021)
Article
Gastroenterology & Hepatology
Mar Coll, Silvia Arino, Celia Martinez-Sanchez, Ester Garcia-Pras, Javier Gallego, Anna Moles, Beatriz Aguilar-Bravo, Delia Blaya, Julia Vallverdu, Teresa Rubio-Tomas, Juan Jose Lozano, Elisa Pose, Isabel Graupera, Andrea Fernandez-Vidal, Albert Pol, Ramon Bataller, Jian-Guo Geng, Pere Gines, Mercedes Fernandez, Pau Sancho-Bru
Summary: The study found that ductular reaction cells promote angiogenesis in chronic liver disease through the Slit2-Robo1 pathway and play a key role in the liver wound-healing response.
Article
Biology
Han Xiao, Tao Zhang, Changjun Li, Yong Cao, Linfeng Wang, Huabin Chen, Shengcan Li, Changbiao Guan, Jianzhong Hu, Di Chen, Can Chen, Hongbin Lu
Summary: Proper mechanical stimulation enhances the migration of Prrx1(+) cells and the release of active TGF-beta 1, promoting the repair of rotator cuff enthesis injuries through ciliary TGF-beta signaling.
Article
Cell Biology
Sirisha Natani, K. K. Sruthi, Sakkarai Mohamed Asha, Priyanka Khilar, Pampana Sandhya Venkata Lakshmi, Ramesh Ummanni
Summary: Neuroendocrine prostate cancer (NEPC) is an aggressive form of prostate cancer that persists even without androgen hormones. This study reveals the role of interleukin-6 (IL-6) in promoting neuroendocrine differentiation (NED) in prostate cancer cells. The TGF-beta signaling pathway, specifically p38MAPK, is identified as the key regulator of IL-6-induced NED. These findings suggest that targeting p38MAPK and its upstream regulators could be a potential therapeutic strategy for treating NEPC.
CELLULAR SIGNALLING
(2022)
