Article
Biochemistry & Molecular Biology
Jisu Jeong, Jiyeon Kim
Summary: EMT plays a crucial role in the development of lung cancer, and targeting EMT could inhibit cancer cell invasion and metastasis. This study found that combination treatment with erlotinib and cilengitide showed enhanced inhibitory effects on EMT in lung cancer cells, suggesting that cilengitide could improve the efficacy of anticancer drugs and contribute to improved treatment strategies for inhibiting EMT-based cancer progression.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2022)
Article
Immunology
Xiaomin Yang, Hongyan Jiang, Jiang Ning, Shufen Zhang, Ying Cai, Liang Wang, Jinsong Yang, Guodong Xu, Wei Chen, Jianfei Wang
Summary: The present study aimed to investigate the sensitivity of G-protein coupled receptor 30 (GPR30) to gefitinib in non-small cell lung cancer (NSCLC) cells. The results showed that GPR30 expression is associated with gefitinib sensitivity, and G15, a GPR30 antagonist, can reduce GPR30 expression and increase sensitivity to gefitinib. Further research demonstrated that G15 or GPR30 siRNA treatment can affect the expression levels of E-cadherin and vimentin.
INTERNATIONAL JOURNAL OF IMMUNOPATHOLOGY AND PHARMACOLOGY
(2023)
Review
Oncology
Jun Ho Lee, Joan Massague
Summary: TGF-beta plays a crucial role in development, wound healing, fibrosis, and cancer by inducing epithelial-mesenchymal transitions (EMTs). EMTs are regulated by multiple signaling inputs, with RAS-MAPK signaling frequently required for EMT induction by TGF-beta. Recent studies have revealed the molecular basis for the cooperation between the TGF-beta-SMAD and RAS-MAPK pathways in EMT induction, offering insights into EMT and progenitor cell differentiation during gastrulation and cancer metastasis.
SEMINARS IN CANCER BIOLOGY
(2022)
Article
Oncology
Xuecong Wang, Pieter Johan Adam Eichhorn, Jean Paul Thiery
Summary: TGF-beta signaling regulates embryonic development, wound-healing, and immune homeostasis, but it is altered during tumor progression, leading to enhanced epithelial cell plasticity and a reprogramming of epithelial cells into mesenchymal lineages through EMT. This contributes to increased carcinoma cell invasion, metastasis, and immune evasion.
SEMINARS IN CANCER BIOLOGY
(2023)
Article
Pharmacology & Pharmacy
Yujin Seo, Minji Seo, Jiyeon Kim
Summary: The cyclic RGD peptides containing aromatic amino acids can inhibit mesenchymal marker expression, migration, and invasion in gefitinib-resistant cells, which may provide a new approach for the treatment of non-small cell lung cancer.
FRONTIERS IN PHARMACOLOGY
(2023)
Article
Integrative & Complementary Medicine
Renyikun Yuan, Qiumei Fan, Xiaowei Liang, Shan Han, Jia He, Qin-Qin Wang, Hongwei Gao, Yulin Feng, Shilin Yang
Summary: This study found that Cucurbitacin B (CuB) can inhibit the process of EMT in lung cancer cells. For TGF-beta 1-induced A549 cells and resistant A549 cells, CuB can inhibit EMT by reducing ROS production and the activity of PI3K/Akt/mTOR signaling pathway. In vivo experiments showed that CuB can effectively inhibit lung cancer metastasis.
Article
Biotechnology & Applied Microbiology
Xuan Wan, Yuting Fang, Jiangzhou Du, Shaoxi Cai, Hangming Dong
Summary: This study found that GW4869 inhibited the expression of eHSP90 alpha, as well as the EMT and invasion abilities of HCC827 and PC9. GW4869 also increased the sensitivity to gefitinib in BALB/c nude mice bearing HCC827 tumors. These findings suggest that GW4869 may enhance gefitinib sensitivity in NSCLC by inhibiting EMT and extracellular HSP90 alpha, providing a new strategy for its treatment.
ONCOTARGETS AND THERAPY
(2023)
Article
Oncology
Yu Liu, Mingxu Da
Summary: This study found that WTAP is significantly overexpressed in gastric carcinoma tissue, and its high expression is closely associated with poor prognosis in gastric cancer patients. Overexpression of WTAP can promote migration and EMT of GC cells, as well as the expression of TGF-beta and mRNA stability. Knockdown of WTAP inhibits migration of GC cells, decreases TGF-beta expression, and reduces mRNA stability. In addition, WTAP also promotes multiple chemotherapy and radiotherapy resistance in GC.
JOURNAL OF CANCER RESEARCH AND CLINICAL ONCOLOGY
(2023)
Review
Medicine, General & Internal
Masao Saitoh
Summary: Epithelial-mesenchymal transition (EMT) plays a crucial role in cancer progression, associated with invasion, metastasis, generation of tumor stem cells, and resistance to therapy. Transforming growth factor (TGF)-beta acts as a key mediator in the EMT process, initiating and maintaining EMT through signaling pathways and transcription factors.
Review
Oncology
Valeria Ramundo, Giuliana Giribaldi, Elisabetta Aldieri
Summary: Metabolic changes in the tumor microenvironment play a critical role in cancer by affecting signaling pathways that control cellular metabolism. The deregulation of cancer metabolism is closely related to oxidative stress control and the involvement of cytokines like transforming growth factor beta (TGF-beta) in tumorigenesis and cancer progression. The crosstalk between TGF-beta and oxidative stress contributes significantly to tumorigenesis and cancer invasiveness by affecting redox imbalance and cellular metabolism.
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
Li Wei, Naiyuan Shao, Ya Peng, Peng Zhou
Summary: The study revealed a correlation between high CTSS expression and glioma tissue grades, with CTSS inhibitor ZFL attenuating TGF-beta-induced invasive growth. Inhibition of CTSS reversed TGF-beta-induced epithelial-to-mesenchymal transition and restored the turnover of tight junction proteins, leading to decreased mobility of glioblastoma cells. Furthermore, the PI3K/AKT/mTOR pathway was found to be suppressed in the TGF-beta+ZFL groups, highlighting its importance in this process.
Article
Ophthalmology
Yi Chen, Binxin Wu, Jian Feng He, Jingyao Chen, Zi Wei Kang, Dandan Liu, Junjie Luo, Kexin Fang, Xiaoxu Leng, Haibin Tian, Jingying Xu, Caixia Jin, Jieping Zhang, Juan Wang, Jingfa Zhang, Qingjian Ou, Lixia Lu, Furong Gao, Guo-Tong Xu
Summary: This study successfully induced EMT in RPE cells through prolonged low-density culture, and found that the combination of the ROCK inhibitor Y27632 and the TGF-beta receptor inhibitor RepSox effectively suppressed and reversed the EMT process, maintaining the morphology and function of RPE cells and the retina. This combined therapy could be a new strategy for treating proliferative retinal diseases involving EMT of RPE cells.
INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE
(2021)
Article
Biochemistry & Molecular Biology
Xiaohong Wu, Haiyan Wang, Huamu Chen, Hongrong Lin, Min Li, Zhihui Yue, Liangzhong Sun
Summary: This study revealed that NPHP1 defects activate the TGF-beta/Smad signaling pathway and EMT in MDCK cells, characterized by decreased expression of E-cadherin and beta-catenin, and increased expression of alpha-SMA and FSP1. These factors may contribute to the pathogenesis of interstitial fibrosis in NPHP.
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
(2021)
Article
Clinical Neurology
Naita M. Wirsik, Jakob Ehlers, Lisa Maeder, Elena I. Ilina, Anna-Eva Blank, Anne Grote, Friedrich Feuerhake, Peter Baumgarten, Kavi Devraj, Patrick N. Harter, Michel Mittelbronn, Ulrike Naumann
Summary: The study found that in glioma-associated pericytes, elevated SLUG expression is mediated by TGF-beta, leading to morphological changes and enhanced proliferation, motility, and altered growth patterns. Downregulation of SLUG or addition of a TGF-beta antagonising antibody abolished these effects, indicating a potential mechanism for tumor vasculature formation and blood-brain barrier breakdown in glioblastoma.
NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY
(2021)