CSNK2A1: A Potential Drug Target and Biomarker for Prostate and Lung Cancer

Target Name: CSNK2A1

NCBI ID: G1457

CSNK2A1

CSNK2A1: A Potential Drug Target and Biomarker for Prostate and Lung Cancer

Introduction

Prostate and lung cancer are two of the leading causes of cancer-related deaths worldwide. The good progression and relatively low resistance to chemotherapy make these two cancers hot areas of drug research. Although many patients still do not receive effective treatment, research is still of great significance in finding new treatments and biomarkers. In recent years, researchers have conducted in-depth studies on the expression and function of the CSNK2A1 gene. On the basis of this finding, this article aims to explore the role of CSNK2A1 in prostate and lung cancer and explore the possibility of CSNK2A1 as a potential drug target and biomarker.

CSNK2A1 gene overview

CSNK2A1 is a transcription factor belonging to the WASP (Wiskott-Aldrich syndrome protein 2) family, and its encoding gene is KLF1 (Kirsten rat sarcoma viral oncogene homolog 1). CSNK2A1 is expressed in a variety of tissues, including prostate, lung, colorectal and ovarian cancer. Studies have found that the expression level of CSNK2A1 is positively correlated with the prognosis of various cancers. In addition, the expression level of CSNK2A1 is also related to chemotherapy resistance and tumor growth rate.

CSNK2A1 function and tumorigenesis

The mechanism of action of CSNK2A1 in tumorigenesis is still not fully understood. However, studies have found that CSNK2A1 is involved in a series of key biological processes in a variety of cancers, including cell cycle regulation, DNA damage repair, cell proliferation and apoptosis. In these processes, CSNK2A1 may play an antioxidant, anti-apoptotic, and anti-tumor proliferation role, thereby playing a key role in tumorigenesis.

The relationship between CSNK2A1 and chemotherapy resistance

Chemotherapy resistance is a serious problem in cancer treatment. Many chemotherapy drugs encounter resistance problems when treating cancer. The role of CSNK2A1 in chemotherapy resistance has been well studied. Studies have found that the expression level of CSNK2A1 is positively correlated with chemotherapy resistance. In addition, CSNK2A1 is also closely related to the metabolism and clearance ability of chemotherapy drugs, which provides new ideas for studying anti-chemotherapy drug strategies.

The relationship between CSNK2A1 and lung cancer

Lung cancer is one of the most common causes of death from cancer. The mechanism of CSNK2A1 in lung cancer has also attracted much attention. Studies have found that CSNK2A1 is up-regulated in lung cancer tissues and cells and is involved in the occurrence and development of lung cancer. In addition, CSNK2A1 is also closely related to the invasion and metastasis ability of lung cancer. These findings provide new targets for research on lung cancer treatment.

The relationship between CSNK2A1 and prostate

Prostate cancer is the most common malignant tumor in men. The mechanism of action of CSNK2A1 in the prostate has also attracted much attention. Studies have found that CSNK2A1 is up-regulated in prostate tissues and cells and is involved in the occurrence and development of prostate cancer. In addition, CSNK2A1 is also closely related to the invasion and metastasis ability of prostate cancer. These findings provide new targets for research into prostate cancer treatments.

CSNK2A1 as a drug target

Based on the mechanism of CSNK2A1 in tumorigenesis, CSNK2A1 has become a research hotspot. Multiple studies have confirmed that CSNK2A1 can be used as a target for anti-tumor drugs. At present, some drugs targeting CSNK2A1 have been widely used in clinical research, such as anti-chemotherapy drugs and anti-tumor vaccines.

However, there are still some challenges in current drug research on CSNK2A1. First, the expression level of CSNK2A1 in tumors is relatively complex, and its expression level is affected by multiple factors, such as age, gender, tumor type, etc. Therefore, these factors need to be fully considered when studying drug targets for CSNK2A1. Secondly, CS

Protein Name: Casein Kinase 2 Alpha 1

Functions: Catalytic subunit of a constitutively active serine/threonine-protein kinase complex that phosphorylates a large number of substrates containing acidic residues C-terminal to the phosphorylated serine or threonine (PubMed:11239457, PubMed:11704824, PubMed:16193064, PubMed:19188443, PubMed:20625391, PubMed:22406621, PubMed:24962073, PubMed:31439799). Regulates numerous cellular processes, such as cell cycle progression, apoptosis and transcription, as well as viral infection (PubMed:12631575, PubMed:19387552, PubMed:19387551). May act as a regulatory node which integrates and coordinates numerous signals leading to an appropriate cellular response (PubMed:12631575, PubMed:19387552, PubMed:19387551). During mitosis, functions as a component of the p53/TP53-dependent spindle assembly checkpoint (SAC) that maintains cyclin-B-CDK1 activity and G2 arrest in response to spindle damage (PubMed:11704824, PubMed:19188443). Also required for p53/TP53-mediated apoptosis, phosphorylating 'Ser-392' of p53/TP53 following UV irradiation. Can also negatively regulate apoptosis (PubMed:11239457). Phosphorylates the caspases CASP9 and CASP2 and the apoptotic regulator NOL3 (PubMed:16193064). Phosphorylation protects CASP9 from cleavage and activation by CASP8, and inhibits the dimerization of CASP2 and activation of CASP8 (PubMed:16193064). Phosphorylates YY1, protecting YY1 from cleavage by CASP7 during apoptosis (PubMed:22184066). Regulates transcription by direct phosphorylation of RNA polymerases I, II, III and IV (PubMed:19387550, PubMed:12631575, PubMed:19387552, PubMed:19387551, PubMed:23123191). Also phosphorylates and regulates numerous transcription factors including NF-kappa-B, STAT1, CREB1, IRF1, IRF2, ATF1, ATF4, SRF, MAX, JUN, FOS, MYC and MYB (PubMed:19387550, PubMed:12631575, PubMed:19387552, PubMed:19387551, PubMed:23123191). Phosphorylates Hsp90 and its co-chaperones FKBP4 and CDC37, which is essential for chaperone function (PubMed:19387550). Mediates sequential phosphorylation of FNIP1, promoting its gradual interaction with Hsp90, leading to activate both kinase and non-kinase client proteins of Hsp90 (PubMed:30699359). Regulates Wnt signaling by phosphorylating CTNNB1 and the transcription factor LEF1 (PubMed:19387549). Acts as an ectokinase that phosphorylates several extracellular proteins (PubMed:19387550, PubMed:12631575, PubMed:19387552, PubMed:19387551). During viral infection, phosphorylates various proteins involved in the viral life cycles of EBV, HSV, HBV, HCV, HIV, CMV and HPV (PubMed:19387550, PubMed:12631575, PubMed:19387552, PubMed:19387551). Phosphorylates PML at 'Ser-565' and primes it for ubiquitin-mediated degradation (PubMed:20625391, PubMed:22406621). Plays an important role in the circadian clock function by phosphorylating BMAL1 at 'Ser-90' which is pivotal for its interaction with CLOCK and which controls CLOCK nuclear entry (By similarity). Phosphorylates CCAR2 at 'Thr-454' in gastric carcinoma tissue (PubMed:24962073). Phosphorylates FMR1, promoting FMR1-dependent formation of a membraneless compartment (PubMed:30765518, PubMed:31439799)

The "CSNK2A1 Target / Biomarker Review Report" is a customizable review of hundreds up to thousends of related scientific research literature by AI technology, covering specific information about CSNK2A1 comprehensively, including but not limited to:
•   general information;
•   protein structure and compound binding;
•   protein biological mechanisms;
•   its importance;
•   the target screening and validation;
•   expression level;
•   disease relevance;
•   drug resistance;
•   related combination drugs;
•   pharmacochemistry experiments;
•   related patent analysis;
•   advantages and risks of development, etc.
The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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