Article
Gastroenterology & Hepatology
Tianhao Weng, Dong Yan, Danrong Shi, Miaojin Zhu, Yizhi Liu, Zhigang Wu, Taoming Tang, Linwei Zhu, Hong Zhang, Hangping Yao, Lanjuan Li
Summary: The study reveals that MSP is an important biomarker in the progression of liver cirrhosis and can be utilized for patient prognostication. The MSP-RON pathway promotes hepatocytes EMT and fibrosis progression via the TGF-beta related pathway. Potential therapeutic strategies for liver cirrhosis targetting the MSP/RON pathway have been identified.
LIVER INTERNATIONAL
(2021)
Article
Biochemistry & Molecular Biology
Hwi Gon Kim, Ye Seon Lim, Seonyeong Hwang, Hye-Yoon Kim, Yuseok Moon, Yong Jung Song, Yong-Jin Na, Sik Yoon
Summary: DEHP, a commonly used plasticizer, may be linked to the development of endometriosis by inducing cell proliferation, migration, inflammation, and stemness through the TGF-β/Smad signaling pathway, providing novel insights into the pathogenesis of endometriosis.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Environmental Sciences
Dapeng Wang, Huifen Xu, Lili Fan, Wenli Ruan, Qian Song, Heng Diao, Rui He, Ying Jin
Summary: Chronic arsenic exposure induces liver fibrosis in rats, which is associated with activation of hepatic stellate cells, excessive extracellular matrix secretion, and hepatocytes epithelial-mesenchymal transformation. Additionally, arsenite exposure causes hyperphosphorylation of EGFR/ERK signaling in liver tissue, suggesting its involvement in arsenic-induced liver fibrosis. Treatment with erlotinib, a specific phosphorylation inhibitor of EGFR, reduces hyperphosphorylation of EGFR/ERK signaling, suppresses hepatocytes EMT, and alleviates liver fibrogenesis in arsenite-exposed rats.
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
(2023)
Article
Medicine, General & Internal
Ritu Shrestha, Kim R. Bridle, Darrell H. G. Crawford, Aparna Jayachandran
Summary: Our study demonstrates a close association between TGF-beta 1-mediated EMT and regulation of immune checkpoints in HCC. Induction of EMT by TGF-beta 1 led to increased migratory potential of HCC cells and upregulation of immune checkpoint molecules PD-L1 and B7-H3, while reversal of EMT resulted in decreased expression of these immune checkpoint molecules.
INTERNATIONAL JOURNAL OF MEDICAL SCIENCES
(2021)
Article
Endocrinology & Metabolism
Xiaobo Ling
Summary: The study revealed that breviscapine suppressed proliferation, migration, invasion, epithelial-to-mesenchymal transition (EMT), and TGF-beta 1/Smad signaling in TGF-beta 1-induced pulmonary fibrotic cells in vitro by blocking the PI3K/AKT/GSK3 beta pathway. This suggests that breviscapine may be a potential candidate for the treatment of pulmonary fibrosis.
JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS
(2022)
Article
Biochemistry & Molecular Biology
Ching-Chung Ko, Yao-Yu Hsieh, Pei-Ming Yang
Summary: Epithelial-to-mesenchymal transition (EMT) is a biological process that promotes cancer cell dissemination and drug resistance. This study revealed that overexpression of MIR31HG in pancreatic ductal adenocarcinoma (PDAC) patients is associated with poorer disease-free survival, as well as upregulation of genes related to TGF beta signaling and EMT. In vitro experiments further demonstrated that TGF beta induces MIR31HG expression and knockdown of MIR31HG reverses TGF beta-induced EMT phenotypes and cancer cell migration.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Biochemistry & Molecular Biology
Tsugumasa Toma, Hiroshi Tateishi, Kensaku Kawakami, Taha F. S. Ali, Masahiro Kamo, Kazuaki Monde, Yuta Nakashima, Mikako Fujita, Masami Otsuka
Summary: Metastasis is the main cause of mortality in solid tumors, but there are no available antimetastatic drugs on the market. This study focused on a synthetic compound called HPH-15, which showed anti-EMT and anti-cell migration activities in non-small-cell lung cancer cells. HPH-15 was found to inhibit downstream TGF-beta signaling and could potentially lead to the development of new antimetastatic drugs.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Cell Biology
Kalliopi Tzavlaki, Yae Ohata, Anita Moren, Yukihide Watanabe, Jens Eriksson, Maiko Tsuchiya, Yuki Kubo, Kouhei Yamamoto, Mikael E. Sellin, Mitsuyasu Kato, Laia Caja, Carl-Henrik Heldin, Aristidis Moustakas
Summary: LKB1 pathway limits TGF beta-induced epithelial-mesenchymal transition, maintaining mammary epithelial morphogenesis. Downregulation of LKB1 expression in breast cancer is predicted to lead to increased epithelial-mesenchymal transition induced by SNAI1 and TGF beta family members.
JOURNAL OF CELLULAR PHYSIOLOGY
(2023)
Article
Biochemistry & Molecular Biology
Ke Li, Rong Zhou, Mingze Ma, Chaomei Jin, Linlin Jiao, Siyu Zhang, Mei Tian, Fang Zhou
Summary: This study demonstrates that TNF-alpha and TGF-beta 1 synergistically promote EMT and cell migration in BEAS-2B cells. In addition, inhibiting the NF-kappa B/NOX4 signaling pathway can suppress the expression of EMT-related markers and cell migration.
MOLECULAR BIOLOGY REPORTS
(2022)
Review
Chemistry, Medicinal
Jianqing Yu, George G. Chen, Paul B. S. Lai
Summary: Hepatocellular carcinoma is a major cause of cancer mortality worldwide, with current treatments showing unsatisfactory outcomes. The HGF/c-Met axis is considered crucial in regulating liver diseases and promoting HCC, and inhibiting this pathway may lead to the development of new and effective treatments for HCC.
MEDICINAL RESEARCH REVIEWS
(2021)
Article
Cell Biology
Joseph L. Mertz, Srinivasa R. Sripathi, Xue Yang, Lijun Chen, Noriko Esumi, Hui Zhang, Donald J. Zack
Summary: Studying kinase/phosphatase signaling cascades in induced EMT of RPE can provide insights into the pathways mediating this process, with liver hyperplasia and HGF-MET signaling showing the highest enrichment. HGF and epidermal growth factor signaling pathways, inhibited by EMT induction, play a role in regulating the RPE transcriptional profile.
Review
Biochemistry & Molecular Biology
Azine Datlibagi, Anna Zein-El-Din, Maxime Frohly, Francois Willermain, Christine Delporte, Elie Motulsky
Summary: Proliferative vitreoretinal diseases (PVDs), such as proliferative vitreoretinopathy (PVR), epiretinal membranes, and proliferative diabetic retinopathy, are characterized by the formation of proliferative membranes due to EMT of retinal pigment epithelium (RPE) and endothelial cells. In vitro models, including cell lines, stem-cell-derived RPE, and primary cells, are utilized to induce EMT and mimic PVD. In vivo PVR animal models are obtained through surgical means or intravitreal injection to investigate EMT and cell behavior. This review provides a comprehensive overview of the current models available for studying EMT in PVD.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Medicine, Research & Experimental
Rui Yu, Yan Wu, Ping He, Yu Bai, Yongzhe Zhang, Xiaohui Bian, Guangping Sun, Beiru Zhang
Summary: Renal fibrosis is the main pathology of chronic kidney disease and LMCD1 is upregulated in patients with CKD and treated kidney cells. Knockdown of LMCD1 can improve renal fibrosis by blocking the activation of the extracellular signal-regulated kinase pathway. The study further investigates the effect of LMCD1 on TGF-01-induced epithelial-mesenchymal transition (EMT) and its potential role in the TGF-01/Smad signaling pathway.
LABORATORY INVESTIGATION
(2023)
Review
Biochemistry & Molecular Biology
Angelique Mottais, Luca Riberi, Andrea Falco, Simone Soccal, Sophie Gohy, Virginia De Rose
Summary: Epithelial-to-mesenchymal transition (EMT) is a reversible process where epithelial cells transform into mesenchymal cells. This transformation is seen in various lung diseases, including lung cancer, interstitial lung diseases, asthma, chronic obstructive pulmonary disease, cystic fibrosis, and bronchiectasis. Chronic inflammation in these diseases can lead to aberrant tissue repair, resulting in structural changes and impaired lung function. Understanding the mechanisms underlying EMT may help identify targets for therapeutic interventions to prevent irreversible structural changes.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2023)
Article
Immunology
Samuel James Brake, Wenying Lu, Collin Chia, Greg Haug, Josie Larby, Ashutosh Hardikar, Gurpreet K. Singhera, Tillie L. Hackett, Mathew Suji Eapen, Sukhwinder Singh Sohal
Summary: COPD is a common respiratory disease characterized by airflow obstruction, and the TGF-β1 and SMAD pathway is believed to be involved in its pathogenesis by inducing epithelial mesenchymal transition (EMT). Smoking and activation of the SMAD pathway were found to be correlated with the decline in lung function in mild to moderate COPD patients, independent of TGF-β1, suggesting the involvement of other factors in driving these pathways.
FRONTIERS IN IMMUNOLOGY
(2023)