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.

Moreover, GAS5 could influence the PTEN/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway. Our study identified GAS5 as a ceRNA that can regulate the PTEN/AKT/mTOR axis by sponging miR-96-5p in OC.

lncRNA FGF14-AS2 was a downregulated lncRNA in prostate carcinoma and influenced cell proliferation and metastasis. The influence relied on modulating miR-96-5p and its target gene AJAP1.

After surgery, collected urine samples showed significantly lower expression of miR-96-5p-: P < 0.001; and miR-183-5p: P = 0.002. In conclusion, urine miR-96-5p and miR-183-5p are promising tumor biomarkers of BC diagnosis; particularly, when they combined with each other or with urinary cytology.

Expression of BCL2 and XIST showed the highest area under ROC curve (AUC), thus potentially having an excellent diagnostic value. Conclusion Based on our expression analyses, it seems that BCL2 — miR-96-5p— XIST axis could be an epigenetic cause of a decreased BCL2 gene expression in high-grade serous ovarian cancer.

Expression of BCL2 and XIST showed the highest area under ROC curve (AUC), thus potentially having an excellent diagnostic value. Conclusion Based on our expression analyses, it seems that BCL2 — miR-96-5p— XIST axis could be an epigenetic cause of a decreased BCL2 gene expression in high-grade serous ovarian cancer.

Expression of BCL2 and XIST showed the highest area under ROC curve (AUC), thus potentially having an excellent diagnostic value. Conclusion Based on our expression analyses, it seems that BCL2 — miR-96-5p— XIST axis could be an epigenetic cause of a decreased BCL2 gene expression in high-grade serous ovarian cancer.

Expression of BCL2 and XIST showed the highest area under ROC curve (AUC), thus potentially having an excellent diagnostic value. Conclusion Based on our expression analyses, it seems that BCL2 — miR-96-5p— XIST axis could be an epigenetic cause of a decreased BCL2 gene expression in high-grade serous ovarian cancer.

Our study suggests that circ-KIAA0907 restrains OSCC progression via the miR-96-5p/UNC13C axis, indicating that it may be a potential target for OSCC treatment.

Ectopic miR-96-5p expression promoted the proliferation and migration of cancer cells in vitro and tumour growth and metastasis in vivo which partially depended on AIMP3. Taken together, our results demonstrated that the axis of miR-96-5p-AIMP3-p53 played an important role in lung adenocarcinoma, which may provide a new strategy for the diagnosis and treatment of NSCLC.

Silencing of secreted frizzled-related protein 4 eliminated the anti-tumor effect of microRNA-96-5p on cervical cancer cells. MicroRNA-96-5p facilitated the viability, migration, and invasion and inhibited the apoptosis of cervical cancer cells via negatively regulating secreted frizzled-related protein 4.

DDAH1 was recognized as a target gene of miR-96-5p, and silencing DDAH1 reversed the effects of miR-96-5p downregulation on the proliferation, migration, invasion and apoptosis of trophoblast cells as well as the expressions of apoptosis-related proteins. MiR-96-5p downregulation promotes proliferation, migration, and invasion, and suppresses apoptosis in human trophoblast cells in vitro via targeting DDAH1, which provides evidence for the implication of miR-96-5p in the functional modulation of trophoblasts.

Levels of miR-96-5p, miR-134-5p, and 181b-5p negatively correlated with the Gleason score. Given further studies, miR-96-5p, miR-134-5p and especially miR-200b-3p and miR-181b-5p may differentiate BPH and PC.

In summary, we are the first to reveal that miR-96-5p inhibits the proliferative, invasive and migratory phenotypes of BCa cells the targeting of CTNND1 and subsequent Wnt/β-catenin signaling. These data highlight miR-96-5p as a novel target for BC treatment.

Moreover, the cell proliferation of LV- miRNA-122-RNAi and LV- miRNA-96-RNAi transfected SaOS2 were significantly decreased compared to the LV- miRNA-122-RNAi-CN and LV- miRNA-96-RNAi group. After adjusting for competing risk factors, we found combined high miRNA-122 and miRNA-96 expression was identified as independent predictor of overall survival.

Analysis of patient cohorts and patient-derived xenografts (PDXs) further demonstrate that the miR-96 may predict sorafenib benefits in HCC patients. Our findings revealed the crucial role of the miR-96 in liver T-ICs expansion and sorafenib response, rendering miR-96 as an optimal target for the prevention and intervention of HCC.

MiR-96-5p was remarkably upregulated in PTC tumor tissues and cells. In addition, it promoted cell growth, invasion, and migration via repressing CCDC67 expression.

Further analyses of the expression of apoptosis-related genes and proteins indicated that miR-96-5p may function to reduce malathion-induced HK-2 cell apoptosis via regulation of the DDIT3/B-cell lymphoma (BCL)-2/caspase-3 signaling pathway. In summary, the results of the present study indicate that miR-96-5p protects HK-2 cells from malathion-induced ER stress-dependent apoptosis by targeting DDIT3.

The presented study showed that upregulation of miR-96-5p inhibited the viability and proliferation of Jurkat T-leukemic cells through suppressing HBEGF expression. Our study provides a novel sight for understanding the pathological mechanism of T-ALL and suggests that miR-96-5p may be a potential biomarker for the therapy and diagnosis of T-ALL.