Adenocarcinoma

ZG16B Protein, Human, Recombinant (E. coli, His) is expressed in E. coli.

ZG16B Protein, Human, Recombinant (His) is expressed in HEK293 mammalian cells with C-10xHis tag. The predicted molecular weight is 20.0 kDa and the accession number is Q96DA0.

Granulocyte-Macrophage Colony Stimulating Factor (GM-CSF) was initially characterized as a growth factor that can support the in vitro colony formation of granulocyte-macrophage progenitors. It is produced by a number of different cell types (including activated T cells, B cells, macrophages, mast cells, endothelial cells and fibroblasts) in response to cytokine of immune and inflammatory stimuli. Besides granulocyte-macrophage progenitors, GM-CSF is also a growth factor for erythroid, megakaryocyte and eosinophil progenitors. On mature hematopoietic, monocytes macrophages and eosinophils. GM-CSF has a functional role on non-hematopoitic cells. It can induce human endothelial cells to migrate and proliferate. Additionally, GM-CSF can also stimulate the proliferation of a number of tumor cell lines, including osteogenic sarcoma, carcinoma and adenocarcinoma cell lines.

Trypsin-3, also known as Trypsin III, brain trypsinogen, Serine protease 3 and PRSS3, is a secreted protein that belongs to the peptidase S1 family. Trypsin-3 PRSS3 is expressed is in pancreas and brain. It contains one peptidase S1 domain. Trypsin-3 PRSS3 can degrade intrapancreatic trypsin inhibitors that protect against CP. Genetic variants that cause higher mesotrypsin activity might increase the risk for chronic pancreatitis (CP). A sustained imbalance of pancreatic proteases and their inhibitors seems to be important for the development of CP. The trypsin inhibitor-degrading activity qualified PRSS3 as a candidate for a novel CP susceptibility gene. Trypsin-3 PRSS3 has been implicated as a putative tumor suppressor gene due to its loss of expression, which is correlated with promoter hypermethylation, in esophageal squamous cell carcinoma and gastric adenocarcinoma.

SMAD3 belongs to the SMAD family. Members of this family mediate signal transduction by the TGF-beta activin BMP-2 4 cytokine superfamily from receptor Ser Thr protein kinases at the cell surface to the nucleus. SMAD3 is involved in cell signalling. It modulates signals of activin and TGFβ's. Binding of SMAD3 with SMAD4 enables its transmigration into the nucleus where it forms complexes with other proteins and acts as a transcription factor. SMAD3 is a receptor-regulated SMAD (R-SMAD). In mice, mutation of SMAD3 has been linked to colorectal adenocarcinoma, increased systemic inflammation, and accelerated wound healing. Increased SMAD3 activity has been implicated in the pathogenesis of scleroderma. Smad3 is also a multifaceted regulator in adipose physiology and the pathogenesis of obesity and type 2 diabetes.

Aberrant STK24 expression was an independent prognostic indicator in lung adenocarcinoma patients. Its dysregulation was associated with its DNA copy number alteration and methylation. STK24 CCM3-regulated exocytosis plays an important role in the protection of kidneys from ischemia-reperfusion injury.

Secreted phosphoprotein 1 (SPP1) expression in TAMs isolated from lung adenocarcinoma tissues and PMA-treated THP-1 cells were measured. Macrophage polarization was identified by flow cytometric analysis. Cell migration and apoptosis were assessed by Transwell migration assays and flow cytometric analysis, respectively. SPP1 is highly expressed in tumor tissues and TAMs isolated from patients with an advanced TNM stage, and also in PMA-treated THP-1 cells.

Fractalkine CX3C chemokine ligand 1 (CX3CL1) is a chemokine involved in the anticancer function of lymphocytes-mainly NK cells, T cells and dendritic cells. Its increased levels in tumors improve the prognosis for cancer patients, although it is also associated with a poorer prognosis in some types of cancers, such as pancreatic ductal adenocarcinoma.

HRas, also known as HRAS, belongs to the small GTPase superfamily, Ras family, and is widely expressed. It functions in signal transduction pathways. HRas can bind GTP and GDP, and they have intrinsic GTPase activity. It undergoes a continuous cycle of de- and re-palmitoylation, which regulates its rapid exchange between the plasma membrane and the Golgi apparatus. Defects in HRAS are the cause of faciocutaneoskeletal syndrome (FCSS). FCSS is a rare condition characterized by prenatally increased growth, postnatal growth deficiency, mental retardation, distinctive facial appearance, cardiovascular abnormalities, tumor predisposition, skin, and musculoskeletal abnormalities. Defects in HRAS also can cause congenital myopathy with excess of muscle spindles. HRAS deficiency may be a cause of susceptibility to Hurthle cell thyroid carcinoma. It has been shown that defects in HRAS can cause susceptibility to bladder cancer which is a malignancy originating in tissues of the urinary bladder. It often presents with multiple tumors appearing at different times and different sites in the bladder. Most bladder cancers are transitional cell carcinomas. They begin in cells that normally make up the inner lining of the bladder. Other types of bladder cancer include squamous cell carcinoma (cancer that begins in thin, flat cells) and adenocarcinoma (cancer that begins in cells that make and release mucus and other fluids). Bladder cancer is a complex disorder with both genetic and environmental influences. Defects in HRAS are the cause of oral squamous cell carcinoma.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy

Endosome lysosome-associated apoptosis and autophagy regulator (ELAPOR1), also known as EIG121 protein, is a type I transmembrane protein induced by estrogen. The estrogen-induced gene 121 (EIG121) has been associated with breast and endometrial cancers,but its mechanism of action remains unknown.May protect cells from cell death by inducing cytosolic vacuolization and upregulating the autophagy pathway. That EIG121 is a good endometrial biomarker associated with a hyperestrogenic state and estrogen-related type I endometrial adenocarcinoma.

CCL16, a chemokine poorly characterized at the functional level. Human CCL16 is a member of the CC family, and its gene maps to human chromosome 17q. In the mouse, only a pseudogene has been identified to date. CCL16 is a functional ligand for CCR1, CCR2, CCR5, and CCR8. Recombinant CCL16 demonstrated chemotactic activity on human monocytes and lymphocytes. Based on the ability of human chemokines to exert activity on and bind to murine receptors, the TSA mouse adenocarcinoma cell line was transfected with human CCL16 cDNA and, in comparison with other cytokines, was shown to be the faster inducer of systemic immune response due to massive, prompt infiltration of leukocytes.Cancer ImmunotherapyImmune CheckpointImmunotherapyTargeted Therapy

GSTA1 (Glutathione S-Transferase Alpha 1) is a Protein Coding gene. This gene encodes a member of a family of enzymes that function to add glutathione to target electrophilic compounds. Glutathione S-transferases (GSTs) are involved in the detoxification of carcinogens and may be linked to carcinogenesis. As a vital component of GSTs, GSTA1 plays an important role in carcinogenesis. GSTA1 expression may be a target molecule in the early diagnosis and treatment of lung cancer. Human colonic adenocarcinoma (Caco-2) cells in culture undergo spontaneous differentiation into mature enterocytes in association with progressive increases in expression of glutathione S-transferase alpha-1 (GSTA1). GSTA1 levels may play a role in modulating enterocyte proliferation but do not influence differentiation or apoptosis. GSTA1 may play a key role during pregnancy.

Secretagogin, also known as SCGN, is a secreted protein that is detectable in human serum after ischemic neuronal damage. It is a recently described calcium-binding protein. Secretagogin SCGN is expressed at high levels in the pancreatic islets of Langerhans and to a much lesser extent in the gastrointestinal tract (stomach, small intestine and colon), the adrenal medulla and cortex and the thyroid C-cells. In the brain, the expression of Secretagogin SCGN is restricted to distinct subtypes of neurons with highest expression in the molecular layer of the cerebellum (stellate and basket cells), in the anterior part of the pituitary gland, in the thalamus, in the hypothalamus and in a subgroup of neocortical neurons. Secretagogin SCGN is widely expressed in prostatic adenocarcinoma as opposed to adenocarcinomas in other organs. The function of Secretagogin SCGN is unknown, but it has been suggested in beta-cells to influence calcium-influx and has been observed downregulated in diabetes-prone BB rat islets exposed to cytokines. Secretagogin SCGN is involved in the calcium metabolism of tumour cells and endothelial cells in a subset of neoplasms of the brain and its coverings. Secretagogin SCGN is also a novel marker for neuroendocrine differentiation.

The miR-137 served as a tumor suppressor in non-small cell lung cancer (NSCLC) and its suppressive effect is mediated by repressing TGFA expression. TGFA gene expression was significantly higher in tumor tissues compared to adjacent normal tissue and high TGFA gene expression strongly correlated with poor survival in patients with lung adenocarcinoma, and miR-374a suppresses lung adenocarcinoma cell proliferation and invasion via targeting TGFA gene expression. Transforming growth factor alpha (TGFA) is a well-characterized mammalian growth factor that might contribute to the development of Cleft lip and palate (CL P).

CD82 antigen, also known as Kai-1, is a widely expressed palmitoylated molecule of the tetraspanin superfamily. KAI1 CD82 is localized on cell membrane and form interactions with other tetraspanins, integrins and chemokines which are respectively responsible for cell migration, adhesion and signaling. CD82 Kai-1 is a component of the promiscuous TIMP-1 interacting protein complex on the cell surface of human adenocarcinoma cells and gives insight into tumorigenic metastatic potential. CD82 Kai-1 suppresses EMT in prostate cancer cells adhered to fibronectin leading to reduced cell migration and invasiveness. CD82 Kai-1 function is important for muscle stem cell function in muscular disorders. Overexpression of CD82 Kai-1 suppresses growth, migration and invasion of oral cancer cells and may be considered as a potential therapeutic target in oral cancer.

Annexin A2 (ANXA2) is a member of the annexin family and has roles in the regulation of cellular growth and in signal transduction pathways. ANXA2 protein is associated with sickle cell osteonecrosis and the expression reduce of ANXA2 is associated with osteosarcoma metastases. ANXA2 functions as an autocrine factor, it can increases osteoclast formation and bone resorption. ANXA2 is involved in muscular dystrophies. In humans, the up-regulation of ANXA2 is related with colon adenocarcinoma cell differentiation.

GNRH2 (Gonadotropin-Releasing Hormone 2) is a Protein Coding gene. This gene is a member of the gonadotropin-releasing hormone (GnRH) gene family. Proteins encoded by members of this gene family are proteolytically cleaved to form neuropeptides which, in part, regulate reproductive functions by stimulating the production and release of the gonadotropins follicle-stimulating hormone (FSH) and luteinizing hormone (LH). 3 alternatively spliced human isoforms have been reported. The second mammalian isoform (GNRH2) is an ineffective stimulant of gonadotropin release. Given that pigs lack testicular GNRHR1, these data may indicate that GNRH2 and its receptor are involved in the autocrine or paracrine regulation of testosterone secretion. Diseases associated with GNRH2 include Colon Mucinous Adenocarcinoma and Ovarian Cancer.

Claudin-18 (CLDN18) is a protein that in humans is encoded by the CLDN18 gene. It belongs to the group of claudins. CLDN18 belongs to the large claudin family of proteins, which form tight junction strands in epithelial cells. CLDN18 plays a major role in tight junction-specific obliteration of the intercellular space, through calcium-independent cell-adhesion activity. CLDN18 has two isoform A1 and isoform A2. Human CLDN18.2 is highly expressed in a signifcant proportion of gastric and pancreatic adenocarcinomas，while normal tissue expression is limited to the epithelium of the stomach. The restricted expression makes it a potential drug target for the treatment of gastric and pancreatic adenocarcinoma, as evidenced by eforts to target CLDN18.2 via naked antibody and CAR-T modalities. IMAB362 (Claudiximab) is a monoclonal antibody against isoform 2 of Claudin-18. It is under investigation for the treatment of gastrointestinal adenocarcinomas and pancreatic tumors. IMAB362 was developed by Ganymed Pharmaceuticals AG.