miR-146a expression

To recapitulate, aprepitant demonstrates a neuroprotective effect against DOX-mediated chemobrain by alleviating inflammatory, oxidative, and apoptotic responses, partly by reducing SP, ER stress, and miR-146a. These findings not only underscore the potential of aprepitant as a neuroprotective agent but also offer new understanding of the mechanisms behind chemobrain, leading to better therapeutic strategies for cancer patients.

MiR-146a shares a pathway with miR-223 through effecting IL-6 expression. Further studies are needed to reveal their impact on EAE and possible applications as drug targets and biomarkers.

Our findings suggest that HT patients have low peripheral blood lncRNA-PVT1 expression and high miR-146a expression. lncRNA-PVT1 and miR-146a level changes were correlated with Th17/Treg cytokine imbalance and could be a potential diagnostic tool and independent influencing factor for HT.

NDK can effectively improve micro-inflammation in CKD ratsby enhancing the release of enterogenous exosomes, thereby enhancing the release of exosome-associated miR-146a and inhibiting micro-inflammation.

Our findings provide further insights into the characterization of CM with specific prognostic features. The graphical abstract was created with BioRender.com.

EMT (N-cadherin, vimentin, E-cadherin) and tumorigenic markers (BRCA1, P53, SOX2) of CSCs decreased after miR-146a inhibition. Bone marrow-derived telocytes and mitochondria derived from telocytes favored the reduction of CSC aggressiveness following this inhibition.

An anti-correlation expression pattern was found among the miR-34a-5p and miR-146a-5p and the respective target hub genes in WA-treated TNBC cells. In conclusion, WA might exert anti-cancer effect in TNBC cells by inducing miR-34a-5p and miR-146a-5p expressions and decreasing CCND1, CDK6, and TARF6 target hub genes in TNBC cells.

Considering the role of doxorubicin in inducing apoptosis and increasing the expression of miR-146a, it can be suggested that this miR is involved in inducing apoptosis in BC cells. In addition, miR-146a can be considered a therapeutic candidate.

These miRNAs can help in distinguishing between ovarian clear cell carcinoma and ovarian endometrioma. To the best of our knowledge, no previous studies have screened any candidates specifically for ovarian clear cell carcinoma.

Through this review, we provide an outline of miR-146a's biogenesis and function, as well as its significant involvement in apoptosis. As well, we investigate the effects of exosomal miR-146a on the promotion of apoptosis in cancer cells and look into how it could possibly help combat chemotherapeutic resistance.

Therefore, our study reveals that miR-146a-5p inhibits the progression of hepatic fibrosis after radiation treatment. And the beneficial role of miR-146a-5p may be relevant to PTPRA-SRC signaling pathway.

We conclude that miR-150 and miR-155 may be potentially applied as prognostic biomarkers in cervical cancer patients. However, further investigation is required to determine their applicability.

This study identified that circMFN2 regulates miR-146a-3p to promote adenoma development partially via the TRAF6/NF-κB pathway and may be a potential therapeutic target for pituitary adenoma.

In conclusion, H. pylori infection may increase the expression of miR-146a and miR-155 in patients with H. pylori and GC positive diagnoses, which can be effective in the curbing the progression of GC. For this reason, up-regulation of miR-146a and miR-155 along with H. pylori infection might contribute to the pathogenesis of GC, and also can be suggested as biomarkers for GC diagnosis and treatment.

In addition to HGSC, tumoral miR-146a expression also correlates strongly with CTL infiltration in other cancer types including thyroid, prostate, breast, and adrenocortical cancers. Altogether, our findings highlight the ability of miR-146a to overcome immune suppression and improve CTL infiltration in tumors.

PIWIL2 may inhibit the progression of TC by sponging miR-146a-3p, providing new insights into the early treatment, recrudescence treatment, and metastasis treatment of TC.

In cultured HPV cells, restoration of miR-146a by forced expression or treatment with miR-146a-loaded sEV, reduced IL-8 level, blocked cell cycle progression, and promoted cell death. These findings identify Dsg2, miR-146a, and IL-8 as potential biomarkers for ICI response and suggest that the Dsg2/miR-146a/IL-8 signaling axis negatively impacts ICI treatment outcomes and could be targeted to improve ICI responsiveness in HPV HNSCC patients.

In contrast, mir196a rs11614913 was not associated with BLCA risk. Therefore, the genotypes of mir146a rs2910164 may serve as a useful biomarker for predicting the risk of BLCA.

In this in vivo MF-like model, particularly useful to study the inflammatory component of MF without driver mutations, dual JAK2+IRAK1 inhibition, with inhibitors such as pacritinib, prevents the development ofthrombocytopenia, splenomegaly, extramedullary hematopoiesis and BM fibrosis, postulated as a potential modifier of the natural course of these diseases. The improvement of inflammatory symptoms in MF patients receiving pacritinib, which does not inhibit JAK1, could be explained by inhibition of the NF-κB pathway through IRAK1. Bone Marrow Fibrosis, Myeloproliferative disorder, Myelofibrosis, NF- B

In addition, the co-culture with resistant cells' exosomes was able to decrease in sensitivity and increase the migration capacities in trastuzumab-sensitive cells, as well as angiogenesis in HUVEC-2 cells. Collectively, these data support the role of miR-146a-5p in resistance to trastuzumab, and demonstrate that it can be transferred by exosomes conferring resistance properties to other cells.

Notably, silencing of Numb could retrieve the self-renewal and migration impaired by knockdown of miR-146a. Our results indicate that miR-146a can regulate the cancer stemness in OSCC by modulating Numb, and hence miR-146a/Numb axis can serve as a potential target for oral cancer therapy.

 Smokeless tobacco leads to salivary overexpression of the miRs 21, 146a, 155, and 199a. Monitoring the levels of these four oncomiRs may provide insight about the future development of oral squamous cell carcinoma, especially in patients with smokeless tobacco habits.

TGF-β was favorably linked with IL-6, cholesterol, triglyceride levels, and BMI. High levels of TGF-β and IL-6 in the blood indicate how intensely inflammation develops in obesity, which could increase the risk of colorectal cancer.

The results indicated that SPP1 is a cancer promoter (oncogene), while PECAM1 and PIK3R1 are cancer suppressor genes. These genes take part in the regulation of biological activities in lung adenocarcinoma, which provides a basis for improving detection and immunotherapeutic targets for lung adenocarcinoma.

NSCLC cells released exosomal miR-146a to inhibit the expressions of TRAF-6 and IRAK-1 in TAMs, resulting in the impaired antitumor activity of TAMs. NSCLC cell-derived exosomal miR-146a represents a novel therapeutic target for NSCLC treatment.

Our results suggest that the level of serum miR-146a can serve as a potential prognostic biomarker for DLBCL patients.

Also, a pilot study indicated differential expression of miR-146a in prostate cancer cell lines and tissues from different racial groups. This report provides a novel insight into understanding the prostate carcinogenesis.

miR-146a evaluation could ameliorate personalized prognosis and support precision medicine decisions in TNBC.

Some non-coding RNAs, such as hsa-miR-146a-5p, are effective in breast cancer targeted therapy. As cancer is a complicated disorder, therefore the combination of therapies might lead to novel therapeutic strategies.

In conclusion, the pro-tumor activity of androgen hormone in melanoma cells could be exacerbated by both miR-146a increase and RNase-L downregulation. These events may contribute to the worse outcome in male melanoma patients.

Aberrant low expression levels of miR-21, miR-18a, and Let-7b derived from serum exosomes exist in patients with MM, which are associated with a worse overall survival rate.

Cel exerts neuroprotective activity against 6-OHDA-caused neurotoxicity by regulating miR-146a/PI3K/Akt/mTOR pathway, which provides a potential application of Cel for treating neurodegenerative diseases.

However, significant correlations between the expressions levels of has-mir-876 and hsa-mir-1269a and patients' prognosis are not found. Our study found that 12 significantly differentially expressed miRNAs might promote the proliferation, invasion, and metastasis of cancer cells by regulating the expression of upstream target genes, thereby affecting the prognosis of patients with endometrial cancer.

Cancer-derived EVs delivered pro-metastatic miR-146a-5p to regulate the actin dynamics in cervical cancer, thereby leading to cancer metastasis. This experiment highlighted an appealing therapeutic modality for cervical cancer.

AVT can inhibit the proliferation, invasion and migration and promote apoptosis of human glioma cells possibly by up-regulating miR-146a expression and inhibiting the PI3K/Akt signaling pathway.

The low expression of miR-146a, miR-182 and miR-200c in HIV+ women could be due to immune exhaustion, viral immune evasive mechanism, or an indicator of viral latency while the higher expression of miR-21; and lower expression of miR-125b and p53 could be early indicators of genetic instability prior to epithelial transformation. Conclusion This study suggests that circulating high expression of miR-21 and low expression of miR-125b and p53 gene could be used in identifying individuals at risk of developing Ca, especially among immunocompromised patients.

This study showed that miR-146a has a stimulatory role in HepG2 cells and promotes HepG2 cell migration and invasion by targeting FLAP mRNA. Thus, miR-146a may be a tumor promoter and a potential therapeutic target for the treatment of HCC patients.

Finally, miR-146a-5p/TRAF6 was found to be involved in the role of HCG18 in GC progression in vivo. Altogether, HCG18 promotes GC progression via the miR-146a-5p/TRAF6 axis and could be a GC treatment target.

Down-regulation of miR-146a may play an important role in the pathogenesis of gastric cancer. The rs2910164 polymorphism of the miR-146a gene may reduce the risk of gastric cancer by influencing the processing of mature miR-146a.