Previous studies have reported that TIFA plays different roles in various tumor types. However, the function of TIFA in colorectal cancer (CRC) remains unclear. Here, we showed that the expression of TIFA was markedly increased in CRC versus normal tissue, and positively correlated with CRC TNM stages. In agreement, we found that the CRC cell lines show increased TIFA expression levels versus normal control. The knockdown of TIFA inhibited cell proliferation but had no effect on cell apoptosis in vitro or in vivo. Moreover, the ectopic expression of TIFA enhanced cell proliferation ability in vitro and in vivo. In contrast, the expression of mutant TIFA (T9A, oligomerization site mutation; D6, TRAF6 binding site deletion) abolished TIFA‐mediated cell proliferation enhancement. Exploration of the underlying mechanism revealed that the protein synthesis‐associated kinase RSK and PRAS40 activation were responsible for TIFA‐mediated CRC progression. In summary, these findings suggest that TIFA plays a role in mediating CRC progression. This could provide a promising target for CRC therapy.

Background: Copper chaperone for superoxide dismutase ( CCS) is an essential component of the oxidation-reduction system. In breast cancer cells, CCS expression is highly up-regulated, which contributes to cellular proliferation and migration. Breast cancer is a multifaceted disease with different tumor prognoses and responses to clinical treatments, which may be associated with multiple molecular subtypes of CCS. Methods: The CCS expression patterns in breast cancer were investigated by TNMplot, cBioPortal, and HPA network database. The correlation of CCS expression with clinicopathological parameters was analyzed using the UALCAN database. The Cancer Genome Atlas (TCGA) data set was used to analyze the Clinical characteristics of CCS in luminal B patients. The bc-GenExMiner database was used to analyze the effects of BReast-CAncer susceptibility gene (BRCA)1/2, TP53 mutation status, estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor (HER) expression on CCS expression. The survival curves and prognostic value of CCS in luminal B breast cancer were performed through Kaplan-Meier curves, univariate and multivariate Cox regression using the PrognoScan, bc-GenExMiner, and Clinical bioinformatics analysis platform. Results: We found that CCS expression was associated with patient age, race, ER, and PR status. We also discovered that BRCA1/2 mutations had an effect on CCS expression. The luminal B subtype had the highest CCS expression, which was linked to poor survival compared with other subtypes. In addition, Kaplan-Meier curve analysis showed that luminal B patients with high CCS mRNA expression showed a poor survival and the CCS gene is an independent predictor of outcome in patients with luminal B breast cancer by univariate and multivariate Cox regression. Conclusions: Our findings emphasize the significant expression of CCS in luminal B breast cancer and its potential as an autonomous prognostic determinant for this specific molecular subtype. These findings suggest that CCS holds promise as a prospective marker for the treatment of luminal B breast cancer.

Purpose: The global incidence and mortality rates associated with cancer are increasing annually, presenting significant challenges in oncology, particularly regarding the efficacy and toxicity of antineoplastic agents. Additionally, mitochondria are recognized for their multifaceted roles in the progression of malignant tumors. Mitochondrial-targeting drugs offer promising avenues for cancer therapy. This study focuses on the synthesis of a mitochondrial fluorescent probe, designated Mitochondrial Probe Molecule-1 (MPM-1), and evaluates its anti-tumor effects on colon cancer (CRC) and lung cancer (LUNG) both in vitro and in vivo.Methods: Mito Tracker Green FM staining was performed to investigate the subcellular location of MPM-1. Cell cycle assay, colony formation, EdU, assay of cell apoptosis, wound healing assay, and trans-well migration assay were utilized to confirm anticancer properties of MPM-1 in vitro. Using a xenograft mouse model, the effects of MPM-1 in tumor treatment were also identified. RNA-seq and Western blot were performed to examine the underlying mechanism of MPM-1.Results: The findings indicate that MPM-1 selectively targets mitochondria and exerts inhibitory effects on CRC and LUNG cells. Specifically, MPM-1 significantly reduced the proliferation and migration of lung cancer cell lines A549 and H1299, as well as colon cancer cell lines SW480 and LOVO, with IC50 values of 4.900, 7.376, 8.677, and 7.720 µM, respectively, while also promoting apoptosis. RNA-seq analysis revealed that MPM-1 exerts its broad-spectrum anticancer effects through interactions with multiple signaling pathways, including mTOR, Wnt, Hippo, PI3K/Akt, and MAPK pathways. Additionally, in vivo studies demonstrated that MPM-1 effectively inhibited tumor progression.Conclusion: In summary, MPM-1 demonstrates the ability to inhibit the growth of CRC and LUNG by targeting mitochondria and modulating several signaling pathways that attenuate tumor cell migration and proliferation while promoting apoptosis. This research underscores the potential of MPM-1 as a tumor suppressor and lays a robust foundation for the future development of innovative anticancer therapies that target mitochondrial functions.

Previous studies have identified several ICAM3 transcript variants and mainly investigated the function of the longest transcript of ICAM3 in various tumor progressions. However, the role of the other ICAM3 transcript variants remains unclear. Herein, we detected the expression of ICAM3 transcript variants 1–4 in DLBCL cells and tumor tissues, disclosed that variants 1, 3, and 4 were expressed in normal B cell lines and 3 DLBCL cell lines except SU-DHL-2 as well as tumor tissues, while variant 2 was not detected. Moreover, we found that ectopic expression of variants 1–4 enhanced cell proliferation by accelerating the cell cycle in SU-DHL2 cells in vitro. In addition, variants 1–4 overexpression showed no effects on SU-DHL2 cell apoptosis. Interestingly, the expression of variants 1, 3, and 4 promoted cell migration and EMT process while variant 2 had no effects. Collectively, the above results displayed the different roles of ICAM3 transcript variants in mediating DLBCL progression.

T-bet is a transcription factor predominantly expressed in immune cells, and it has been associated with a range of physiological and pathological processes, including the differentiation of various immune cell types, the development of immune-related diseases, and tumor progression. Despite notable advancements in the field, current research on T-bet remains fragmented, primarily concentrating on functional studies within specific cell types or the progression of particular diseases. This review aims to provide a comprehensive synthesis of the most recent findings regarding the role of T-bet in various diseases, with an emphasis on elucidating its molecular mechanisms and potential clinical applications. We underscore the involvement of T-bet in the pathogenesis of systemic diseases, including autoimmune disorders, infectious diseases, allergic conditions, endocrine disorders, psychiatric illnesses, and chromosomal abnormalities. Furthermore, we summarize its role in the development of various malignant tumors, such as esophageal cancer, gastric cancer, breast cancer, colon cancer, prostate cancer, and hematological malignancies. Additionally, we discuss the impact of T-bet on several critical processes in tumor biology, including tumor cell proliferation, apoptosis, epithelial-mesenchymal transition (EMT), metastasis, immune cell infiltration, and iron-induced apoptosis. We also assess the potential of T-bet as a prognostic and therapeutic target for tumors. In conclusion, T-bet may serve as a significant biomarker for the diagnosis and treatment of immune disorders and cancer, as well as a target for innovative immunotherapeutic strategies aimed at addressing tumors and immune-related diseases.