miR-96 expression

In conclusion, the present study demonstrated that the Cell Rich TM system combined with the negative enrichment strategy can effectively detect CTCs in the peripheral blood of gastric cancer patients and that the expression of miR-96 can be used as an effective indicator to predict CTC status and assist in determining the prognosis of gastric cancer. These findings have important implications for the diagnosis and treatment of gastric cancer and provide new clues for the further study of the tumor immune microenvironment and tumor heterogeneity.

Our results demonstrated that the novel UCA1/miR-96-5p/Osx pathway regulates osteogenic differentiation of hPDLSCs and sheds new insights and targets for periodontitis therapeutics.

Pearson correlation analysis yielded significantly negative correlations between miR-96-5p and THBS1 (P < .006, r = -0.339), between miR-29b-3p and THBS1 (P < .05, r = -0.421). Our study suggests that miR-96-5p- and miR-29b-3p-mediated THBS1 inhibition is associated with sunitinib resistance in ccRCC, offering a better understanding of the mechanism elucidating acquired drug resistance in ccRCC.

Cybb re-expression in Zeb1-deficient cDC1 fully restores the defective cross-presentation while microRNA-96/182 overexpression in Zeb1-sufficient cDC1 inhibits cross-presentation. Therefore, our results identify a Zeb1-microRNA-96/182-Cybb pathway that controls cross-presentation in cDC1 and uncover an essential role of Zeb1 in cDC1 homeostasis.

HOXA5 silencing had the opposite effects with miR-96-5p inhibition. In conclusion, these results suggest that miR-96-5p is involved in permethrin-promoted proliferation and migration of breast cancer cells by targeting HOXA5.

Our results demonstrate that miR96 and miR182 over-expressions inhibit GBM motility by regulating cytoskeleton through spastin and palladin. These findings suggest that miR96 and miR182 should be investigated in more detail for their potential use in GBM therapy.

Circ_TEX2 could suppress the growth of xenograft tumors in vivo. Our study demonstrates the tumor-suppressive role of circ_TEX2 in hepatoma through miR-96-5p/SPRED1 axis, suggesting that strategies directed toward restoring the production of circ_TEX2 might have a therapeutic value for hepatoma treatment.

These findings demonstrate that LDB2 can act as a new regulator to inhibit cell proliferation, invasion, and metastasis via the ERK1/2 signaling pathway, and miR-96-5p may be a potential promising molecular by targeting LDB2 in lung cancer.

TRIM52-AS1 inhibition or IGF2BP2 overexpression neutralized the inhibition of silencing miR-96-5p on CC cell resistance to DDP. Overall, miR-96-5p improved CC cell resistance to DDP by inhibiting TRIM52-AS1 and promoting IGF2BP2.

The expression patterns of both LINC01314 and miR-96 may be diagnostic of, and prognostic for, CRC. These findings will facilitate further exploration of the molecular mechanism of lncRNAs in CRC.

Existing research suggests a potential role of AnxA1 in the metastasis and immune landscape of TNBC tumors. Preclinical and clinical experiments are warranted to investigate the feasibility and effectiveness of targeting AnxA1 in TNBC.