MX2 (MX Dynamin Like GTPase 2)

Collectively, RBMX2 is a novel host factor that enhances M. bovis infection and drives infection-induced EMT. These findings provide new insight into TB pathogenesis and highlight RBMX2 as a potential target for TB vaccine and therapeutic development.

A Kaplan-Meyer analysis of patients from whom 20 ESCC cell lines or 18 ESCC tissue samples were obtained indicated that EMX2 expression was a poor prognostic marker. EMX2 has a unique function in ESCC stemness and its expression is the stamped marker of poor prognosis in ESCC patients.

In addition, we construct an N1-TANs marker, MX2, which positively correlates with better prognosis in LSCC patients, and employ deep learning techniques to predict expression of MX2 from hematoxylin-eosin (H&E)-stained images so as to conveniently guide decision making in clinical practice. Collectively, our findings demonstrate that the N1-TANs/fibroblasts defense wall formed in response to MTC effectively combat LSCC.

Hence, the orchestrated effects mediated by EMX2-CADM1 axis promote RCC cell death and suppresse its growth and invasion, providing potential intervention strategies for combating RCC. Implications: The EMX2-CADM1 transcriptional axis offers a promising therapeutic target for inducing cell death and inhibiting growth and invasion in renal cell carcinoma, which could lead to more effective treatment strategies for this aggressive malignancy.

In this study, we validate the regulation of DNA methylation on empty spiracles homeobox 2 (emx2) expression with decitabine treatment in Chinese tongue sole testis cells...Taken together, we developed the first DNA methylation editing system in marine species and demonstrated its effective editing ability in Chinese tongue sole cells. This provides a new strategy for both epigenetic research and molecular breeding of marine species.

Knockdown of TMX2 enhanced the anti-tumor effect of lenvatinib. In conclusion, our findings emphasize the pivotal role of TMX2 in driving the HCC cell viability by promoting both autophagy and mitophagy. These results suggest that TMX2 May serve as a prognostic marker and promising therapeutic target for HCC treatment.

Furthermore, EMX2 could significantly attenuate the interaction between Akt and FOXO3a. Taken together, our results demonstrated that EMX2 could inhibit ccRCC progress through, at least in part, modulating Akt/FOXO3a signaling pathway, thus representing a novel role and underlying mechanism of EMX2 in the regulation of ccRCC progress.

We developed the CERPI for effectively predicting survival and response to immunotherapy in patients, and these results may provide guidance for CRC diagnosis and precise treatment.

The findings of this study may elucidate the biological roles of TMX family genes as potential targets for pan-cancer and also offer valuable insights for further investigating how these genes function in the development and spreading of cancer.

The tumor suppressor circ_ATAD3B prevents cancer progression by regulating the miR-570-3p/MX2 pathway. Circ_ATAD3B may be a candidate for targeted therapy of breast cancer.

RNA-Seq was used to investigate the underlying mechanism, which suggests that the TMX2 gene may be crucial in Cu(II) regulation of UPR by inhibiting the activation of GRP78/BiP and PERK/eIF2?. The synergistic antitumor efficacy of CuET-Lipid@Cela via inhibition of TMX2 was also confirmed in a myrAKT/YapS127A plasmid-induced primary CCA mouse model, providing new insights into the reversal of acquired chemotherapy-induced resistance in CCA.

The overexpression of miR-653-5p could reverse the inhibitory effect of EMX2OS on LUAD cells. In conclusion, EMX2OS served as a biomarker in LUAD that indicated patients' prognosis and regulated cellular processes via regulating miR-653-5p.