| Source: HalifaxProj(inhibit) |
| Type: |
| (Prev called GRO1 oncogene)(KC) belongs to the CXC The chemokine ligand 1 (CXCK1) is a small peptide belonging to the CXC chemokine family that acts as a chemoattractant for several immune cells, especially neutrophils or other non-hematopoietic cells to the site of injury or infection and plays an important role in regulation of immune and inflammatory responses. CXCL1 is increased in ovarian cancer via GRB2-associated binding protein 2-dependent autocrine way, promoting tumour cells proliferation and angiogenesis; Keratinocyte-derived chemokine (KC) belongs to the CXC family and it is homologous to interleukin (IL)-8. The CXC chemokines can be further divided into two main subgroups based on the presence or absence of the ELR (Glu-Leu-Arg) motif: 1. ELR+ CXC Chemokines: These include chemokines such as CXCL1, CXCL2, CXCL3, CXCL5, CXCL6, CXCL7, CXCL8 (IL-8), and CXCL12 (SDF-1). They are primarily involved in promoting angiogenesis, recruiting neutrophils, and facilitating tumor growth. 2. ELR- CXC Chemokines: This subgroup includes chemokines like CXCL4, CXCL9, CXCL10, and CXCL11. These chemokines are often associated with anti-tumor immunity and can attract T cells and other immune cells to the tumor microenvironment. CXC chemokines, particularly the ELR+ subset, can promote tumor growth by enhancing angiogenesis. CXC chemokines are involved in the metastatic spread of cancer cells. For example, CXCL12 and its receptor CXCR4 are known to play significant roles in the migration of cancer cells to distant sites, such as the bone marrow and lymph nodes. Given their roles in cancer progression, CXC chemokines and their receptors are being investigated as potential therapeutic targets. |
| Cyclooxygenase (COX)-2 overexpression has been noted in various cancers.
PI3Ks/AKT pathways are over-activated in several types of cancers. EGFR altered activity has been noted in various pathological conditions. However, its regulation is an important step in the inhibition of cancer. In this regard, EGCG shows a pivotal role in the inhibition of EGFR activity. Activating protein-1 transcription factor has been associated with pathogenesis including cancer. Activation of the sonic hedgehog (Shh) pathway is required for the growth of numerous tissues and organs and recent evidence indicates that this pathway is often recruited to stimulate growth of cancer stem cells (CSCs) and to orchestrate the reprogramming of cancer cells via epithelial mesenchymal transition (EMT). Increased expression of Nanog has been associated with the aggressive nature of certain cancers, highlighting its role in promoting cancer stem cell characteristics. The aberrant hedgehog (Hh)/GLI signaling pathway causes the formation and progression of a variety of tumors. The process of cell apoptosis is often accompanied by the destruction of mitochondrial transmembrane potential, which is widely regarded as one of the earliest events in the process of cell apoptosis. Human malignancies frequently exhibit mutations in the TGF-β pathway, and overactivation of this system is linked to tumor growth by promoting angiogenesis and inhibiting the innate and adaptive antitumor immune responses50. Several studies have demonstrated that high cyclin D1 expression was observed in cancers including breast, lung, prostate, lymph node and colorectal cancers [23–25]. The oncogene c-myc, which is frequently over-expressed in cancer cells, is involved in the transactivation of most of the glycolytic enzymes including lactate dehydrogenase A (LDHA) and the glucose transporter GLUT1 [51,52]. Thus, c-myc activation is a likely candidate to promote the enhanced glucose uptake and lactate release in the proliferating cancer cell. Vimentin is overexpressed in various epithelial cancers, including prostate cancer, gastrointestinal tumors, tumors of the central nervous system, breast cancer, malignant melanoma, and lung cancer. Vimentin’s overexpression in cancer correlates well with accelerated tumor growth, invasion, and poor prognosis; however, the role of vimentin in cancer progression remains obscure. Heat shock proteins (HSPs) are normally induced under environmental stress to serve as chaperones for maintenance of correct protein folding but they are often overexpressed in many cancers, including breast cancer. Since NQO1 is highly expressed in many solid tumors, including via upregulation of Nrf2, the design of compounds activated by NQO1 and NQO1-targeted drug delivery have been active areas of research. Since increased Nrf2 gene expression is one of the main mechanisms of cancer cells in resisting chemotherapeutic drugs and survival in oxidative conditions; finding compounds with the ability to suppress Nrf2 gene expression with minimum side effects can be considered an important strategy for increasing the sensitivity of cancer cells to chemotherapy. Overexpression of c-met stimulates proliferation, migration and invasion in various types of cancer including prostate cancer. Overexpression of TGFα and EGFR by many carcinomas correlates with the development of cancer metastasis, resistance to chemotherapy and poor prognosis. More than 50% of human cancers have a mutated nonfunctional p53. |
| 2819- | CUR, | Chemo, | Curcumin as a hepatoprotective agent against chemotherapy-induced liver injury |
| - | Review, | Var, | NA |
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