Knocking Down SKA1 Inhibits Hepatocellular Carcinoma Progression via Apoptosis: Integrating Single-Cell Transcriptomics With In Vivo and In Vitro Validation
Contact us if these videos are not relevant.
Contact us if these videos are not relevant.
View abstract on PubMed
Summary
This summary is machine-generated.Knocking down Spindle- and kinetochore-associated complex 1 (SKA1) inhibits hepatocellular carcinoma (HCC) progression by promoting apoptosis. This study found high SKA1 expression correlates with poor HCC prognosis and identified SKA1
Area Of Science
- Oncology
- Molecular Biology
- Genetics
Background
- Hepatocellular carcinoma (HCC) is the most common primary liver cancer.
- Spindle- and kinetochore-associated complex 1 (SKA1) is implicated in mitosis and cancer progression.
- The role of SKA1 in HCC pathogenesis requires further elucidation.
Purpose Of The Study
- To investigate the impact of SKA1 knockdown on HCC progression.
- To analyze SKA1 expression, patient survival, and prognostic associations in HCC.
- To explore SKA1's role in immune cell infiltration, gene mutation, and cellular communication in HCC.
Main Methods
- Bioinformatic analyses including single-cell transcriptome sequencing.
- In vitro experiments: CCK-8, wound healing, Transwell, flow cytometry, qRT-PCR.
- In vivo studies measuring tumor growth; Western blot for protein expression.
Main Results
- High SKA1 expression is linked to poor HCC survival, prognosis, TP53 mutation, and immune cell infiltration.
- SKA1 knockdown suppressed HCC cell viability, invasion, migration, and tumor growth.
- SKA1 knockdown induced cell cycle arrest, promoted apoptosis, and modulated apoptosis-related protein expression.
Conclusions
- SKA1 knockdown inhibits HCC progression by enhancing apoptosis signaling.
- SKA1 represents a potential therapeutic target for hepatocellular carcinoma.
- Understanding SKA1's role in cell communication and apoptosis is crucial for HCC treatment strategies.
Contact us if these videos are not relevant.
Contact us if these videos are not relevant.
Related Concept Videos
The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...