miR-340 expression

SZ-685C caused a decrease in PPP1CB expression and activation of the ERK pathway in PDFS cells, and this trend was reversed after overexpression of miR-340-3p. SZ-685C downregulates the expression of miR-340-3p in PDFS cells, thereby reducing the expression of PPP1CB and activating the ERK pathway to promote autophagic cell death, leading to inhibition of PDFS cell growth.

Knocking down CircCCND1 can inhibit the malignant behaviors of lung cancer H446 cells, which may be achieved through the regulation of miR-340-5p/TGIF1 axis.

As for the results of multivariate analysis, disease stage, risk level (high risk), high MVD, low miR-340 expression, and high miR-155 expression were all independent risk factors for CML resistance. MVD and the expression of miR-340 and miR-155 are closely associated with CML resistance after TKI treatment.

Furthermore, miR-340 CNPs caused down-regulation of BRP-39 (breast regression protein-39) increasingly suggested as a prognostic biomarker for neoplastic diseases like BC. In conclusion, our data show that miR-340 CNPs can be considered as a promising new platform for BC gene therapy.

CENPL potentially regulated by miR-340-3p, is overexpressed in PAAD and predicts patient's prognosis, suggestive of a diagnostic and prognostic value in PAAD patients.

These findings provide novel perceptions about the mechanisms of the KD, curcumin, and ODE to cure gastric cancer. It suggested that the KD as adjunctive therapy along with conventional therapies in traditional medicine could be considered a useful solution to prevent and treat gastric cancer.

PERK or ATF6 overexpression dramatically attenuated phenotypes of miR-340-5p up-regulation. Altogether, miR-340-5p targets the endoplasmic reticulum stress proteins PERK and ATF6 to affect OSCC cell proliferation and invasion.

In conclusion, miR-340 functions as a tumor suppressor of BC, which inhibited proliferation and induced apoptosis by targeting Glut-1 partly through regulating PCNA, Bax expression and PI3K/AKT pathway. This study suggested that miR-340 is a potential target for the treatment of BC.

Confocal microscopy confirmed that the reduction of FHL2 expression by miR-340-5p mimic also reversed serum-induced E-cad disruption and that the target site blocker abrogated the effect of miR-340-5p. The current results suggested that miR-340-5p could be used to antagonize colon cancer cell metastasis by targeting the FHL2-E-cad axis.

miR-141 and miR-340 expressions are associated with PTEN expression (P = 0.002 and P < 0.001). miR-141 and miR-340 may be associated with their target gene PTEN and involved in the carcinogenesis of cervical squamous epithelium.

MiR-340-5p repressed the malignant phenotypes of OS via targeting NRF2 and regulating PI3K/AKT pathway and EMT. The current study provided preclinical evidence for the potential applications of miR-340-5p/NRF2 axis in OS therapies.

miR-340 was downregulated, whereas CCND1 was upregulated in LC tissues, and the expression levels of the two genes were closely related to the prognosis and clinicopathological characteristics of LC.

The FZD3 silencing abrogated the inhibitory effect of miR-340 knockdown on cell proliferation, migration, invasion, Ala level, and glycolysis level in 786-O cells. In conclusion, miR-340 promotes proliferation, migration, and invasion of RCC cells via suppressing FZD3 expression, and the promotion effect of miR-340 on RCC progression may be due to its regulatory effect on glycolysis and Ala level.

And SChLAP1/EZH2 could also promote prostate cancer tumor development via the interaction of microRNA-DNMT3a signaling pathways in xenograft nude mice. Altogether, our results suggest that SChLAP1 enhanced the proliferation, migration, and tumorigenicity of prostate cancer cells through interacting with EZH2 to recruit H2K27me3 and mediate promoter methylation modification of miR-340-5p/miR-143-3p/miR-145-5p with a DNMT3a-feedback loop.

Moreover, SNHG3 could bind with miR-340-5p and reduce its expression levels, and miR-340-5p attenuated SNHG3-induced tumor proliferation and HOXA10 expression in NSCLC cells. Our findings unveiled that SNHG3 might be an oncogenic factor in NSCLC by downregulating miR-340-5p.

In vivo, aspirin reduced the growth of xenografted tumors. In conclusion, the present study indicated that aspirin partially inhibited cholangiocarcinoma cell proliferation and tumor growth by inducing G0/G1 phase cell cycle arrest, potentially through the miR‑340‑5p/cyclin D1 axis.