TMBIM6 (Transmembrane BAX inhibitor motif-containing protein 6)

Overall, these results indicate that the DHRS4-AS1/hsa-miR-222-3p/TMBIM6 axis is involved in the progression of PRAD and may act as a prognostic biomarker. Our results provide a foundation for further experimental validation and potential clinical translation.

miR-542-3p upregulation or TMBIM6 downregulation counter-balanced the pro-tumor effects of hsa_circ_0000520 overexpression. hsa_circ_0000520 promotes BC proliferation and metastasis through miR-542-3p-targeted TMBIM6.

Further, the RNA-binding mutant of CSDE1 showed reduced affinity towards TMBIM6 mRNA, thus allowing AGO2-mediated silencing of TMBIM6 expression. Our study highlights the pivotal role of CSDE1 in regulating miR-20a-5p function and the expression of TMBIM6 in melanoma cells, thus unveiling the potential of therapeutic strategies targeting this regulatory pathway in treating malignant skin cancers.

Taken together, our findings provide novel evidences that LicoD exerts anti-melanoma effects by down-regulation of BI-1(TMBIM6)/AKT signaling pathways in vitro and in vivo. These findings suggest essential insights for the future development of strategies in skin cancer prevention and treatment.

Despite its promise, the zebrafish xenograft model remains underutilized in Ca2+-related metastasis research. Future work using transgenic lines like tg-EGFP:flk1 and tg-GCaMP, CRISPR knockouts, morpholinos or optogenetic approaches could unlock deeper insights and guide novel metastasis-targeting therapies.

The bladder cells were overexpressed or silenced with TCF3/TMBIM6 with ferroptosis inducer (Erastin)/Ca2+ blocker (BAPTA-AM) to investigate the effects on Ca2+-dependent ferroptosis and other functions...Our findings demonstrate that TCF3 facilitates bladder cancer progression through the enhancement of TMBIM6-Ca2+-mediated ferroptosis resistance. Both TCF3 and TMBIM6 emerge as promising biomarkers and therapeutic targets for bladder cancer intervention.

Additionally, hsa-miR-128-3p was identified as an upstream regulator of TMBIM6. These findings highlight TMBIM6's potential as a prognostic biomarker for glioma, offering new insights into its role in glioma progression.

The PHB2Ser91/Ser176 phosphorylation axis regulated by PIEZO1-TMBIM6 is an important target for LIG nano-drug delivery systems to improve mitochondrial damage in DIC.

In summary, our comprehensive multiomics analysis of CLL patients undergoing ibrutinib therapy has unveiled early immunomodulatory effects on T cells and adaptative mechanisms in CLL cells. These findings can contribute to the identification of resistance mechanisms and the discovery of novel therapeutic targets.

Silencing XIST upregulates miR-329-3p, leading to the suppression of TMBIM6 expression and inhibition of NSCLC progression. These findings suggest that the XIST/miR-329-3p/TMBIM6 axis could serve as a promising molecular target for therapeutic strategies in NSCLC.

Finally, we provide in vivo proof of concept for clinical application, whereby TCRMART1 T cells promote cancer cell killing by TCRTMBIM6W>F.1 T cells through the generation of W>F neoepitopes. Thus, neoepitopes arising from W>F substitution present shared and highly expressed immunogenic targets with the potential to overcome current limitations in adoptive T cell therapy.

Here, we also present the validation of cancer signatures based on direct high-throughput reverse transcription-PCR. Our large survey of lung tumors presents a rich data resource that may help to understand molecular subtypes of lung tumor between AAs and EAs and reveal new therapeutic vulnerabilities that potentially advance health equity.