AIM2 promotes the progression of HNSCC via STAT1 mediated transcription and IL-17/MAPK signaling.

Chronic inflammation has been recognized as one of the hallmarks of head and neck squamous cell carcinoma (HNSCC), Absent In Melanoma 2(AIM2) has emerged as important regulators of chronic inflammatory, and participated in initiation, progression of kinds of human cancers. Nonetheless, the biological functions and underlying mechanisms of AIM2 in HNSCC remain inadequately understood. Based on the bioinformatics analysis of public databases, we identified elevated AIM2 expression in HNSCC, which positively correlates with disease stage and HPV infection, thereby possessing both diagnostic and prognostic significance.

Conditional knockout of the NSD2 gene in mouse intestinal epithelial cells inhibits colorectal cancer progression.

Background: Nuclear receptor-binding SET domain 2 (NSD2) is a histone methyltransferase, that catalyzes dimethylation of lysine 36 of histone 3 (H3K36me2) and is associated with active transcription of a series of genes. NSD2 is overexpressed in multiple types of solid human tumors and has been proven to be related to unfavorable prognosis in several types of tumors.

Methods: We established a mouse model in which the NSD2 gene was conditionally knocked out in intestinal epithelial cells.

Anti-apoptotic protein BCL-XL as a therapeutic vulnerability in gastric cancer.

Background: New therapeutic targets are needed to improve the outcomes for gastric cancer (GC) patients with advanced disease. Evasion of programmed cell death (apoptosis) is a hallmark of cancer cells and direct induction of apoptosis by targeting the pro-survival BCL2 family proteins represents a promising therapeutic strategy for cancer treatment. Therefore, understanding the molecular mechanisms underpinning cancer cell survival could provide a molecular basis for potential therapeutic interventions.

Signal Amplification Pretargeted PET/Fluorescence Imaging Based on Human Serum Albumin-Encapsulated GdF Nanoparticles for Diagnosis of Ovarian Cancer.

Different modal imaging techniques could be complementary in tumor diagnosis. Human serum albumin (HSA)-encapsulated GdF nanoparticles were developed as T1 magnetic resonance imaging (MRI) contrast agents. However, no significant T1 enhancement in the tumor site of the SKOV3 human ovarian cancer xenograft tumor model was observed within 3 h after injection of tetrazine-modified GdF@HSA NPs through small-animal MRI.

Loss of endothelial EMCN drives tumor lung metastasis through the premetastatic niche.

Background: Metastasis is the primary cause of cancer-related mortality. Metastasis involves a complex multistep process during which individual tumor cells spread primarily through destruction of the endothelial barrier, entering the circulatory system to colonize distant organs. However, the role of the endothelial barrier as the rate-limiting process in tumor metastasis and how these processes affect the regulation of the host microenvironment at the molecular level are poorly understood.

Heterogeneous nuclear ribonucleoprotein K promotes the progression of lung cancer by inhibiting the p53-dependent signaling pathway.

Background: Heterogeneous nuclear ribonucleoprotein K (hnRNPK) is a nucleic acid-binding protein. Reportedly, hnRNPK is overexpressed in many human tumors, and such overexpression is associated with poor prognosis, implicating the role of hnRNPK as an oncogene during tumorigenesis. In this study, hnRNPK expression in lung cancer tissues was investigated.

Real-time imaging reveals specific nanoparticle target binding in a syngeneic glioma mouse model.

Nanomaterial-based drug delivery is a promising strategy for glioma treatment. However, the detailed dynamics of nanoparticles in solid glioma are still a mystery, including their intratumoral infiltration depth, penetration, retention time, and distribution. Revealing these processes in detail requires repeated intravital imaging of the corresponding brain tumor regions over time during glioma growth.

Uncovering the interplay between pH receptors and immune cells: Potential drug targets (Review).

Extracellular acidosis is associated with various immunopathological states. The microenvironment of numerous solid tumours and inflammatory responses during acute or chronic infection are all related to a pH range of 5.5‑7.

Novel spontaneous myelodysplastic syndrome mouse model.

Background: Myelodysplastic syndrome (MDS) is a group of disorders involving hemopoietic dysfunction leading to leukemia. Although recently progress has been made in identifying underlying genetic mutations, many questions still remain. Animal models of MDS have been produced by introduction of specific mutations.

Inhibition of host Ogr1 enhances effector CD8 T-cell function by modulating acidic microenvironment.

Immunotherapies for cancer, such as immune checkpoint blockade or adoptive T-cell transfer, can lead to a long-lasting clinical response. But the therapeutic response rate remains low on account of many tumors that have evolved sophisticated strategies to evade immune surveillance. Solid tumors are characterized by the highly acidic microenvironment, which may weaken the effectiveness of antitumor immunity.

Summary of animal models of myelodysplastic syndrome.

Myelodysplastic syndrome (MDS) is a malignant tumor of the hematological system characterized by long-term, progressive refractory hemocytopenia. In addition, the risk of leukemia is high, and once it develops, the course of acute leukemia is short with poor curative effect. Animal models are powerful tools for studying human diseases and are highly effective preclinical platforms.

Research progress on the structure and function of endomucin.

Endomucin is a type I integral membrane glycoprotein, which is expressed in venous and capillary endothelial cells. It consists of 261 amino acids with an extracellular domain that is highly -glycosylated at serine and threonine residues and has several potential -glycosylation sites. Endomucin plays an important role in biological processes such as cell interaction, molecular cell signaling, angiogenesis and cell migration, and in recent years it has also been identified as an anti-adhesion molecule and a marker of endothelial cells.

Involvement of the Wnt/β-Catenin signaling pathway in the heterogenous nuclear ribonucleoprotein K-driven inhibition of proliferation and migration in head and neck squamous cell carcinoma.

The abnormal upregulation of heterogeneous nuclear ribonucleoprotein K (hnRNP K) expression levels were reported to be involved in the progression of various types of cancer. Therefore, it is hypothesized that hnRNP K may serve as a useful diagnostic marker and antitumor target; however, only a few studies to date have investigated the exact role of hnRNP K in head and neck squamous cell carcinoma (HNSCC) and the potential downstream signaling pathway involved. The present study aimed to identify the roles of hnRNP K in the proliferation and migration of HNSCC, and the possible signaling pathways hnRNP K may be associated with in HNSCC.

Downregulation of HNRNPK in human cancer cells inhibits lung metastasis.

Background: Lung cancer frequently occurs in the clinic, leading to poor prognosis and high mortality. Markers for early diagnosis of lung cancer are scarce, and further potential therapeutic targets are also urgently needed.

Method: We established a new mouse model in which the specific gene HNRNPK (heterogeneous nuclear ribonucleoprotein K) was downregulated after administration of doxycycline.

HNRNPK inhibits gastric cancer cell proliferation through p53/p21/CCND1 pathway.

Gastric cancer (GC) is one of the most common human cancers. The molecular mechanisms underlying GC carcinogenesis and progression are still not well understood. In this study, we showed that heterogeneous nuclear ribonucleoprotein K (HNRNPK) was an effective prognostic marker for GC patients especially in early stage.

Smurf1 targets Securin for ubiquitin-dependent degradation and regulates the metaphase-to-anaphase transition.

The HECT E3 ligase Smurf1 (Smad ubiquitination regulatory factor 1) plays a critical role in several important biological pathways by targeting many proteins for ubiquitination and degradation, such as Smad1/5, MEKK2 and RhoA. However, the function of Smurf1 in metaphase-to-anaphase transition remains unclear. Here, we show that Smurf1 interacts with and targets Securin, an inhibitor of sister-chromatid separation, for poly-ubiquitination and proteasomal degradation.

Smurf1 controls S phase progression and tumorigenesis through Wee1 degradation.

Smad ubiquitination regulatory factor 1 (Smurf1) is a HECT-type E3 ubiquitin ligase that regulates several important signaling pathways, including the bone morphogenetic protein pathway and the transforming growth factor-beta (TGF-β) signaling pathway. However, the function of Smurf1 in cell cycle progression remains unclear. Here, we demonstrate that silencing of Smurf1 results in S phase arrest, confirming that Smurf1 is required for S phase progression.

Research Advances in the Mechanisms of Gastric Cancer Multidrug Resistance.

Gastric cancer is one of the most common human malignancies and the third cause of death from cancer in China and worldwide. Chemotherapy is still one of the major treatment options for advanced gastric cancer. However,the efficacy of chemotherapy for gastric cancer remains poor due to its insensitivity and the development of multidrug resistance (MDR).