VIM expression

Additionally, silencing NKD2 restored the anticarcinogenic phenotype associated with IFIX overexpression, affecting cell proliferation, invasion and migration. These findings provide mechanistic insights into the antioncogenic effects of IFIX in OSCC, involving the inhibition of Wnt signalling through NKD2, which leads to cancer-inhibiting phenotypic effects, including restricted EMT.

This, in turn, promoted EMT, facilitating cytoskeleton remodeling-stimulated metastasis and chemoresistance to DDP. Overall, these findings provided a new perspective on the role of CCND3 in LUAD progression and acquired cisplatin resistance.

Circ_0002232 and circ-VIM could be valuable diagnostic biomarkers to differentiate AML patients from healthy controls in clinical use. Circ-VIM expression may influence AML prognosis. Further research is needed to validate the clinical utility of circ_0002232 as a prognostic marker for OS in AML patients.

IGSF1 promotes EMT and metastasis in EC through the upregulation of the c-Myc expression. IGSF1 may serve as a potential therapeutic target for EC, and its inhibition can offer new strategies for mitigating the aggressiveness and metastatic potential of this malignancy.

STEAP3 was significantly associated with CC progression mediated via the JAK/STAT3 signaling pathway and may serve as an effective therapeutic target.

Further, CLP36 silencing repressed the expressions of Cadherin 2 (CDH2) and Vimentin (VIM) yet promoted those of Bax and Caspase 3 in lymphoma cells, concurrent with the reduction on the phosphorylation of PI3K, AKT and CREB, all of which were confirmed to be positively correlated with CLP36. This study, so far as we are concerned, provided evidence on the involvement of CLP36/PI3K/AKT/CREB axis in lymphoma, which may be contributive for the identification on the relevant molecular targets of lymphoma.

The findings of this study indicate that exosomal lncRNA H19 could be a diagnostic marker for Breast Cancer and these Breast cancer exosomes can induce malignant phenotype in fibroblasts and turn them into CAFs. Botox-A could be toxic for both normal fibroblasts and CAFs, inducing apoptosis and suppressing cell proliferation among them.

Furthermore, in human clear cell renal cell carcinoma (ccRCC) samples, we found a negative correlation between KPC1 and vimentin expression. Overall, we demonstrate that the KPC1 ubiquitin E3 ligase downregulates vimentin expression, thereby reducing migration and tumorigenicity of cancer cells.

High expression of CRTAC1 in GC tissues affects immunotherapeutic efficacy and prognosis of the patients, possibly by promoting epithelial-mesenchymal transition via modulating tumor mutational load, tumor microenvironment, and the PI3K/AKT signaling pathway.

Both migration and invasion rate of the cancer cells transfected with METTL3-shRNA were significantly decreased. These findings highlight the pro-oncogenic function of METTL3 in colorectal and melanoma cancer cells, indicating that inhibiting METTL3 could be a promising approach for tumor suppression across multiple cancer types; nonetheless, further investigation is essential to confirm these observations.

In addition, aberrant glycosylation was observed in BBR-M-10-treated CCA cell lines, as evidenced by the low expression level of surface Sambucus Nigra lectin-binding α2,6-sialylated glycans and the reduction of α2,6 sialyltransferase gene expression levels after BBR-M-10 treatment in CCA cell lines. These findings suggested that black rice bran-derived anthocyanins could potentially be used as anti-metastatic agents against CCA.

In vivo experiments demonstrated that TEFM knockout effectively suppressed the growth of subcutaneous glioma xenografts in nude mice. Collectively, these findings highlight the critical role of TEFM in GBM growth and invasion, suggesting that it could serve as a promising therapeutic target for glioma treatment.