ArticleAmerican journal of cancer research2026
PDGF-BB secreted by OTSCC orchestrates CAF-driven tumor progression through regulating the LINC00886/hsa-miR-15b-5p/AKT axis.
Article in American journal of cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Under the induction of factors derived from tumor cells, fibroblasts can transform into cancer-associated fibroblasts (CAFs), in which non-coding RNAs play a key role. This study aims to reveal the regulatory mechanisms of long non-coding RNAs (lncRNAs) in CAFs induced by PDGF-BB from oral tongue squamous carcinoma cells. This study found that PDGF-BB effectively induces the transformation of fibroblasts into cancer-associated fibroblasts (CAFs). Through focused analysis of transcriptional results, it was discovered that LINC00886 is significantly overexpressed in CAFs (PDGF-BB). Furthermore, knocking down LINC00886 in CAFs (PDGF-BB) resulted in a reversal of related CAF markers, including downregulation of CAF marker proteins, reduced lactate secretion, and inhibition of aerobic glycolysis. Additionally, as a long non-coding RNA, LINC00886 regulates cellular biological behaviors through interactions with miRNAs. Predictions from the ENCORI online database revealed that LINC00886 can interact with hsa-miR-15b-5p. Further analysis indicated that the AKT-mTOR signaling pathway is inhibited in the transcriptome data of CAFs with knocked-down LINC00886. When an inhibitor of hsa-miR-15b-5p was added to CAFs (sh-LINC00886), the total AKT protein level was significantly upregulated, and the phosphorylation level of mTOR was also upregulated. This result was confirmed in a xenograft model. Our study demonstrates that PDGF-BB induces the transformation of fibroblasts into CAFs and thereby promotes tumor progression by regulating the LINC00886/hsa-miR-15b-5p/AKT signaling axis, providing new potential targets for cancer therapy.
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