The oncoprotein, hepatitis B X-interacting protein (HBXIP), has been reported to play an important role in human malignancies. However, its functions in non-small cell lung cancer (NSCLC) are poorly understood. The goal of the present study was to identify the role of HBXIP in the regulation of NSCLC development.

The level of HBXIP expression in NSCLC tissue was assessed by immunohistochemical and Western blot analyses, and its relationships with clinicopathological features and outcomes were statistically evaluated. The effects of HBXIP on NSCLC cell progression were assessed through cell viability, colony formation, and flow cytometry analyses

. The mechanism by which HBXIP regulated the MAPK pathway was studied by Western blot, immunofluorescence, and immunoprecipitation assays. In addition,

experiments were performed to evaluate the progression of NSCLC and ERK signaling pathway activation after HBXIP knockdown.

HBXIP was overexpressed in human NSCLC and was correlated with the invasiveness of teraction promoted oncogenesis via the MAPK/ERK pathway, which may serve as a novel therapeutic target for cancers in which MAPK/ERK signaling is a dominant feature.

, which encodes the Bystin protein in humans, is upregulated in reactive astrocytes following brain damage and/or inflammation. GSK2126458 mw We aimed to determine the role and mechanism of BYSL in glioma cell growth and survival.

BYSL expression in glioma tissues was measured by quantitative real-time PCR, Western blot, and immunohistochemistry.

assays were performed to assess the role of BYSL in cell proliferation and apoptosis. Protein interactions and co-localization were determined by co-immunoprecipitation and double immunofluorescence. The expression and activity of the AKT/mTOR signaling molecules were determined by Western blot analysis, and the role of BYSL in glioma growth was confirmed in an orthotopic xenograft model.

The BYSL mRNA and protein levels were elevated in glioma tissues. Silencing BYSL inhibited glioma cell proliferation, impeded cell cycle progression, and induced apoptosis, whereas overexpressing BYSL protein led to the opposite effects. We identified a complex consisting of BYSL, RIOK2, and mTOR, and observed co-localization and positive correlations between BYSL and RIOK2 in glioma cells and tissues. Overexpressing BYSL or RIOK2 increased the expression and activity of AKT/mTOR signaling molecules, whereas downregulation of BYSL or RIOK2 decreased the activity of AKT/mTOR signaling molecules. Silencing BYSL or RIOK2 decreased the growth of the tumors and prolonged the lifespan of the animals in an orthotopic xenograft model.

High expression of BYSL in gliomas promoted tumor cell growth and survival both

and

These effects could be attributed to the association of BYSL with RIOK2 and mTOR, and the subsequent activation of AKT signaling.

High expression of BYSL in gliomas promoted tumor cell growth and survival both in vitro and in vivo. These effects could be attributed to the association of BYSL with RIOK2 and mTOR, and the subsequent activation of AKT signaling.

The newly defined cancer-testis (CT) gene,

was previously found to play key roles in DNA double-strand break (DSB) repair. In this study, we aimed to investigate the effects and mechanisms of MEIOB in the carcinogenesis of triple-negative breast cancers (TNBCs).

The Cancer Genome Atlas database was used to quantify the expression of

. Cox regression analysis was used to evaluate the association between

expression and the prognosis of human TNBC. The effects of MEIOB on cell proliferation and migration in TNBCs were also assessed

. Patient-derived xenograft (PDX) models were used to assess the sensitivity of breast cancers with active MEIOB to PARP1 inhibitors.

We confirmed

as a CT gene whose expression was restricted to the testes and breast tumors, especially TNBCs. Its activation was significantly associated with poor survival in breast cancer patients [overall, hazard ratio (HR) = 1.90 (1.16-2.06); TNBCs HR = 7.05 (1.16-41.80)]. In addition, we found that

was oncogenic and significantly promoted the proliferation of TNBC cells. Further analysis showed that

participated in DSB repair in TNBCs. However, in contrast to its function in meiosis, it mediated homologous recombination deficiency (HRD) through the activation of polyADP-ribose polymerase (PARP)1 by interacting with YBX1. Furthermore, activated MEIOB was shown to confer sensitivity to PARP inhibitors, which was confirmed in PDX models.

played an oncogenic role in TNBC through its involvement in HRD. In addition, dysregulation of

sensitized TNBC cells to PARP inhibitors, so

may be a therapeutic target of PARP1 inhibitors in TNBC.

MEIOB played an oncogenic role in TNBC through its involvement in HRD. In addition, dysregulation of MEIOB sensitized TNBC cells to PARP inhibitors, so MEIOB may be a therapeutic target of PARP1 inhibitors in TNBC.Intermittent fasting (IF) is becoming a prevailing topic worldwide, as it can cause changes in the body’s energy metabolism processes, improve health, and affect the progression of many diseases, particularly in the circumstance of oncology. Recent research has shown that IF can alter the energy metabolism of tumor cells, thereby inhibiting tumor growth and improving antitumor immune responses. Furthermore, IF can increase cancer sensitivity to chemotherapy and radiotherapy and reduce the side effects of these traditional anticancer treatments. IF is therefore emerging as a promising approach to clinical cancer treatment. However, the balance between long-term benefits of IF compared with the harm from insufficient caloric intake is not well understood. In this article, we review the role of IF in tumorigenesis and tumor therapy, and discuss some scientific problems that remain to be clarified, which might provide some assistance in the application of IF in clinical tumor therapy.Natural killer/T-cell lymphoma (NKTCL) is a highly invasive subtype of non-Hodgkin lymphoma, typically positive for cytoplasmic CD3, CD56, cytotoxic markers, including granzyme B and TIA1, and Epstein-Barr virus (EBV). The current treatment methods for NKTCL are associated with several drawbacks. For example, chemotherapy can lead to drug resistance, while treatment with radiotherapy alone is inadequate and results in frequent relapses. Moreover, hematopoietic stem cell transplantation exhibits limited efficacy and is not well recognized by domestic and foreign experts. In recent years, immunotherapy has shown good clinical results and has become a hot spot in cancer research. Clinical activity of targeted antibodies, such as daratumumab (anti-CD38 antibody) and brentuximab vedotin (anti-CD30 antibody), have been reported in NKTCL. Additionally, dacetuzumab and Campath-1H have demonstrated promising results. Further encouraging data have been obtained using checkpoint inhibitors. The success of these immunotherapy agents is attributed to high expression levels of programmed death-ligand 1 in NKTCL.