NLRX1: a key regulator in mitochondrial respiration and colorectal cancer progression.

Colorectal cancer (CRC) is a prevalent and aggressive malignancy with high mortality rates and significant risks to human well-being. Population-wide screening for tumor suppressor genes and oncogenes shows promise for reducing the incidence and fatality of CRC. Recent studies have suggested that NLRX1, an innate immunity suppressor, may play a role in regulating chronic inflammation and tumorigenesis.

Id2 epigenetically controls CD8 T-cell exhaustion by disrupting the assembly of the Tcf3-LSD1 complex.

CD8 T-cell exhaustion is a state of dysfunction that promotes tumor progression and is marked by the generation of Slamf6 progenitor exhausted (Tex) and Tim-3 terminally exhausted (Tex) subpopulations. Inhibitor of DNA binding protein 2 (Id2) has been shown to play important roles in T-cell development and CD8 T-cell immunity. However, the role of Id2 in CD8 T-cell exhaustion is unclear.

Targeting the up-regulated CNOT3 reverses therapeutic resistance and metastatic progression of EGFR-mutant non-small cell lung cancer.

Lung cancer is the leading cause of cancer-related mortality worldwide. CNOT3, a subunit of the CCR4-NOT complex, has recently been suggested to be overexpressed in lung cancer and involved in tumor malignancy. However, its precise role and the underlying mechanisms still need to be fully revealed.

Large HBV Surface Protein-Induced Unfolded Protein Response Dynamically Regulates p27 Degradation in Hepatocellular Carcinoma Progression.

Up to 50% of hepatocellular carcinoma (HCC) is caused by hepatitis B virus (HBV) infection, and the surface protein of HBV is essential for the progression of HBV-related HCC. The expression of large HBV surface antigen (LHB) is presented in HBV-associated HCC tissues and is significantly associated with the development of HCC. Gene set enrichment analysis revealed that LHB overexpression regulates the cell cycle process.

SMURF2 facilitates ubiquitin-mediated degradation of ID2 to attenuate lung cancer cell proliferation.

SMAD-specific E3 ubiquitin protein ligase 2 (SMURF2) functions as either a tumor promoter or tumor suppressor in several tumors. However, the detailed effect of SMURF2 on non-small cell lung cancer has not been fully understood. In this study, SMURF2 expression and its diagnostic value were analyzed.

Regulatory Mechanisms and Reversal of CD8T Cell Exhaustion: A Literature Review.

CD8T cell exhaustion is a state of T cell dysfunction during chronic infection and tumor progression. Exhausted CD8T cells are characterized by low effector function, high expression of inhibitory receptors, unique metabolic patterns, and altered transcriptional profiles. Recently, advances in understanding and interfering with the regulatory mechanisms associated with T cell exhaustion in tumor immunotherapy have brought greater attention to the field.

Integrative and Comprehensive Pan-Cancer Analysis of Lymphocyte-Specific Protein Tyrosine Kinase in Human Tumors.

Lymphocyte-specific protein tyrosine kinase (LCK) is common in a variety of hematologic malignancies but comparatively less common in solid tumors. This study aimed to explore the potential diagnostic and prognostic value of LCK across tumors through integrative and comprehensive pan-cancer analysis, as well as experimental validation. Multiple databases were used to explore the expression, alteration, prognostic value, association with immune infiltration, and potential functional pathways of LCK in pan-cancers.

[Research progress in metabolic reprogramming of endothelial cells and T cells and potential therapeutic targets for chronic inflammation].

Metabolic reprogramming plays a very important role in the immunoregulatory process, and T cells, as the indispensable part in the immune response, realize the change of function and state through metabolic reprogramming. And endothelial cells exhibit similar metabolic reprogramming. This review explores the interaction between endothelial cells and T cells to reveal the mechanism of the former as non-professional antigen presenting cells to recruit and activate the latter and the specific mechanism of cytokines produced by the latter in inflammatory response to regulate the function and state of the former, aiming to find the potential therapeutic targets for chronic inflammation and provide new ideas for the treatment.

Viruses Run: The Evasion Mechanisms of the Antiviral Innate Immunity by Hantavirus.

Hantavirus can cause hemorrhagic fever with renal syndrome (HFRS) in Eurasia and hantavirus pulmonary syndrome (HPS) in America, with high mortality and unknown mechanisms. Innate immunity is the host's first-line defense to bridge the acquired immunity against viral infections. However, hantavirus has evolved various strategies in both molecular and cellular aspects to evade the host's natural immune surveillance.

[Knockdown of NLRC3 promotes proliferation and invasion of human colon cancer cells].

Objective To investigate the effects of nucleotide binding oligomerization domain-like receptor family caspase recruitment domain containing 3 (NLRC3) on the proliferation, migration and invasion of human colon cancer HCT116 and LoVo cells. Methods NLRC3 was knocked down in HCT116 and LoVo cells by NLRC3-specific siRNA (si-NLRC3). NLRC3 mRNA and protein expression was detected by real-time quantitative PCR and Western blotting.

[Rho GTPase-activating protein 11A (ARHGAP11A) is up-regulated in lung adenocarcinoma and positively associated with poor prognosis].

Objective To clarify the expression and clinical significance of ARHGAP11A in lung adenocarcinoma. Methods The expression of ARHGAP11A in lung adenocarcinoma and normal tissue was obtained and analyzed by searching online databases such as Oncomine, and bioinformatic analysis was carried out on the relevant clinicopathological parameters and survival data of lung cancer patients. PrognoScan prognostic analysis database was used to analyze the relationship between ARHGAP11A gene expression and prognosis of lung adenocarcinoma.

HTNV infection of CD8 T cells is associated with disease progression in HFRS patients.

Hantaan viruses (HTNVs) are zoonotic pathogens transmitted mainly by rodents and capable of infecting humans. Increasing knowledge of the human response to HTNV infection can guide the development of new preventative vaccines and therapeutic strategies. Here, we show that HTNV can infect CD8 T cells in vivo in patients diagnosed with hemorrhagic fever with renal syndrome (HFRS).

Vaccines and Therapeutics Against Hantaviruses.

Hantaviruses (HVs) are rodent-transmitted viruses that can cause hantavirus cardiopulmonary syndrome (HCPS) in the Americas and hemorrhagic fever with renal syndrome (HFRS) in Eurasia. Together, these viruses have annually caused approximately 200,000 human infections worldwide in recent years, with a case fatality rate of 5-15% for HFRS and up to 40% for HCPS. There is currently no effective treatment available for either HFRS or HCPS.

Incorporation of CD40 ligand or granulocyte-macrophage colony stimulating factor into Hantaan virus (HTNV) virus-like particles significantly enhances the long-term immunity potency against HTNV infection.

Purpose: Hantavirus infections cause severe haemorrhagic fever with renal syndrome (HFRS) in humans and are associated with high fatality rates. In 2017, numerous outbreaks were reported in China and Germany. This represents a significant public-healthcare issue with no effective HFRS vaccines that offer a long-term immune response.