Diffuse invasion is an important factor leading to treatment resistance and a poor prognosis in gliomas. Herein, we found that expression of the tripartite motif containing 56 (TRIM56), a RING-finger domain containing E3 ubiquitin ligase, was markedly higher in glioma than in normal brain tissue, and was significantly correlated with malignant phenotypes and a poor prognosis. In vitro and in vivo experimental studies revealed that TRIM56 promoted the migration and invasion of glioma cells. Mechanistically, TRIM56 was transcriptionally regulated by SP1 and promoted the K48-K63-linked poly-ubiquitination transition of IQGAP1 at Lys-1230 by interacting with it, which in turn promoted CDC42 activation. This mechanism was confirmed to mediate glioma migration and invasion. In conclusion, our study provides insights into the mechanisms through which TRIM56 promotes glioma motility, i.e., by regulating IQGAP1 ubiquitination to promote CDC42 activation, which might be clinically targeted for the treatment of glioma.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9985612 | PMC |
| http://dx.doi.org/10.1038/s41419-023-05702-6 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Andrographolide Mitigates Cisplatin Resistance by Inhibiting SPP1 Regulated NF-kB/iNOS/COX-2 and PI3K/AKT Pathway in Cisplatin Resistant Cervical Carcinoma Cells.
Drug Dev Res
February 2025
Department of Genetics & Biotechnology, University College of Science, Osmania University, Hyderabad, Telangana, India.
Drug resistance and cancer recurrence are major cause of Cervical cancer (CC) patient mortality. Cisplatin (CDDP) is the major drug that has been extremely used in all stages in treating CC, although relapse and malignant instances have been observed as a result of cisplatin resistance in CC. In the present study, we established Cisplatin resistant CC HeLa cell line model and the cytotoxic effects of Andro as a single agent or in combination with CDDP were investigated to assess its potential as a chemotherapeutic agent in cisplatin-resistant HeLa (CisR-HeLa) cells.
View Article and Find Full Text PDFRhoA and Rac1 as Mechanotransduction Mediators in Colorectal Cancer.
Adv Biol (Weinh)
January 2025
Queensland Micro- and Nanotechnology Centre, Nathan Campus, Griffith University, Brisbane, QLD, 4111, Australia.
Colorectal cancer (CRC) remains a leading cause of cancer-related deaths, creating an urgent need for innovative diagnostic solutions. Mechanobiology, a cutting-edge field that investigates how physical forces influence cell behavior, is now revealing new insights into cancer progression. This research focuses on two crucial players: RhoA and Rac1, small yet powerful proteins that regulate the structure and movement of cancer cells.
View Article and Find Full Text PDFSubcellular Cavitation Bubbles Induce Cellular Mechanolysis and Collective Wound Healing in Ultrasound-Inflicted Cell Ablation.
Adv Sci (Weinh)
January 2025
Institute of Biomechanics and Medical Engineering, Applied Mechanics Laboratory, Department of Engineering Mechanics, School of Aerospace Engineering, Tsinghua University, Beijing, 100084, China.
Focused ultrasound (FUS) has been widely adopted in medical and life science researches. Although various physical and biological effects of FUS have been well-documented, there is still a lack of understanding and direct evidence on the biological mechanism of therapeutic cell ablation caused by high-intensity ultrasound (HIFU) and the subsequent wound healing responses. This study develops an enclosed cell culture device that synergistically combines non-invasive FUS stimulation and real-time, on-the-fly live-cell imaging, providing an in vitro platform to explore short and long-term biological effects of ultrasound.
View Article and Find Full Text PDFAlda‑1 restores ALDH2‑mediated alcohol metabolism to inhibit the NF‑κB/VEGFC axis in head and neck cancer.
Int J Mol Med
April 2025
Department of Medical Education and Research, Kaohsiung Veterans General Hospital, Kaohsiung 813414, Taiwan, R.O.C.
The adaptation of cancer cells to hostile environments often necessitates metabolic pathway alterations to sustain proliferation and invasion. Head and neck cancer (HNC) has unfavorable outcomes. Therefore, elucidating the functional effects and molecular mechanisms underlying metabolic changes is key.
View Article and Find Full Text PDFTriptolide reverses cis‑diamminedichloroplatinum resistance in esophageal squamous cell carcinoma by suppressing glycolysis and causing mitochondrial malfunction.
Mol Med Rep
March 2025
Department of Thoracic Surgery, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.
The present study investigated the sensitization mechanism of triptolide (TPL) in esophageal squamous cell carcinoma (ESCC) resistant to cis‑diamminedichloroplatinum (CDDP). CDDP‑resistant TE‑1/CDDP and KYSE30/CDDP cells were created using an incremental drug concentration approach. TPL and CDDP treatment conditions were screened based on the Cell Counting Kit‑8 cell viability assay and cell proliferation was detected using 5‑ethynyl‑2'‑deoxyuridine and clone formation assays.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!