Effect and potential mechanism of oncometabolite succinate promotes distant metastasis of colorectal cancer by activating STAT3
These videos have been matched automatically. Contact us if they are not relevant.
These videos have been matched automatically. Contact us if they are not relevant.
View abstract on PubMed
Summary
This summary is machine-generated.Oncometabolite succinate significantly increases colorectal cancer cell migration and invasion. It promotes the epithelial-mesenchymal transition (EMT) process by activating STAT3, leading to cancer metastasis.
Area Of Science
- Oncology
- Biochemistry
Background
- Oncometabolites, such as succinate, are increasingly recognized for their role in cancer progression.
- Elevated succinate levels have been observed in various cancers, but its specific impact on colorectal cancer (CRC) metastasis requires further elucidation.
Purpose Of The Study
- To investigate the role of oncometabolite succinate in promoting colorectal cancer cell migration and invasion.
- To explore the underlying molecular mechanisms, including the epithelial-mesenchymal transition (EMT) and STAT3 signaling pathway.
Main Methods
- Succinate levels were quantified in tumor and adjacent tissues using a detection kit.
- Colorectal cancer cell lines (SW480, HCT116) were treated with succinate, and their migration and invasion capabilities were assessed via wound-healing and Transwell assays.
- Epithelial-mesenchymal transition (EMT) markers and STAT3/p-STAT3 expression were analyzed using Western blot and qRT-PCR.
- In vivo metastasis models in mice were utilized to validate findings.
Main Results
- Succinate levels were significantly higher in colorectal carcinoma tissues compared to adjacent tissues.
- Succinate treatment enhanced migration and invasion of CRC cells, promoted EMT biomarker expression, and increased STAT3 phosphorylation (p-STAT3).
- In vivo studies confirmed that succinate promotes EMT and distant metastasis in mice by increasing p-STAT3 expression.
Conclusions
- Succinate acts as an oncometabolite that drives colorectal cancer progression.
- Succinate promotes CRC cell migration, invasion, and metastasis by inducing EMT via STAT3 activation.
- Targeting the succinate-STAT3-EMT axis may offer a therapeutic strategy for colorectal cancer.
These videos have been matched automatically. Contact us if they are not relevant.
These videos have been matched automatically. Contact us if they are not relevant.
Related Concept Videos
Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...