ArticleTranslational cancer research2019
CD147 promotes glucose metabolism, invasion and metastasis via PI3K/AKT pathway in oral squamous cell carcinomas.
Article in Translational cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- CD147/Basigin: From Integrative Molecular Hub to Translational Therapeutic Target.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Current nano drug delivery systems for targeting head and neck squamous cell carcinoma microenvironment: a narrative review.Molecular biology reports · 2025Review
- Hypoxia signaling in cancer: HIF-1α stimulated by COVID-19 can lead to cancer progression and chemo-resistance in oral squamous cell carcinoma (OSCC).Discover oncology · 2025Review
- Dysregulated PI3K/AKT signaling in oral squamous cell carcinoma: The tumor microenvironment and epigenetic modifiers as key drivers.Oncology research · 2025Review
- The adhesin RadD enhances Fusobacterium nucleatum tumour colonization and colorectal carcinogenesis.Nature microbiology · 2024Article
- The Multiple Roles of CD147 in the Development and Progression of Oral Squamous Cell Carcinoma: An Overview.International journal of molecular sciences · 2022Review
- Physalin A Suppresses Human Oral Squamous Carcinoma Cell Migration and Invasion Through Inhibiting Grb2/Ras and MMP/uPA Signaling Pathways.In vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe incidence of oral cancers, especially that of oral squamous cell carcinoma (OSCC), has increased significantly in the last few decades. Aggressive tumor progression and metastasis are the key factors responsible for the high mortality rate associated with OSCC. CD147 is known to play a key role in tumor metastasis and is associated with poor prognosis in oral cancer. It is also a crucial regulator of glucose metabolism in cancer cells. The aim of this study was to determine the effect of CD147 on OSCC invasiveness, metastasis and glucose metabolism, as well as the underlying mechanism.
methodsCD147 was knocked down in the human OSCC lines SCC-25 and CAL-27, and both the wild-type and knockdown cells were then stably transfected with PI3K cDNA. Glucose metabolism and in vitro migration of the OSCC cells were respectively analyzed by glucose uptake and lactate secretion assays, and transwell assay.
resultsKnocking down CD147 in the OSCC cells significantly reduced their migration, and decreased glucose metabolism. The inhibitory effects of blocking CD147 were reversed upon PI3K overexpression.
conclusionsCD147 mediates its oncogenic effects via the PI3K/AKT pathway, and is a potential prognostic factor and therapeutic target for OSCC.
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