C-FOS inhibition promotes pancreatic cancer cell ferroptosis by transcriptionally regulating the expression of SLC7A11
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.Cellular proto-oncogene C-Fos promotes pancreatic cancer growth by upregulating SLC7A11, inhibiting ferroptosis. Targeting C-Fos may offer a new therapeutic strategy for pancreatic ductal adenocarcinoma (PAAD).
Area Of Science
- Oncology
- Molecular Biology
- Biochemistry
Background
- The proto-oncogene C-Fos is a component of the AP-1 transcription factor, implicated in various malignancies.
- Its specific role in pancreatic ductal adenocarcinoma (PAAD) pathogenesis is not well-defined.
- Understanding C-Fos function is crucial for developing novel PAAD therapies.
Purpose Of The Study
- To investigate the role of C-Fos in pancreatic adenocarcinoma (PAAD) progression.
- To elucidate the molecular mechanisms by which C-Fos influences PAAD cell behavior.
- To evaluate C-Fos as a potential therapeutic target for PAAD.
Main Methods
- Bioinformatic analysis, RT-PCR, and Western Blotting (WB) to assess C-Fos expression in PAAD.
- Short hairpin RNA (shRNA) mediated C-Fos knockdown in PANC-1 and BxPC-3 cell lines.
- Chromatin Immunoprecipitation (ChIP) and Dual-luciferase assays to determine C-Fos's transcriptional regulation of SLC7A11.
- In vivo studies using a xenograft nude mouse model.
Main Results
- C-Fos expression was elevated in PAAD tissues and cells.
- C-Fos depletion inhibited PAAD cell proliferation and induced ferroptosis.
- C-Fos directly binds to the SLC7A11 promoter, upregulating its transcription.
- SLC7A11 overexpression counteracted the effects of C-Fos knockdown on proliferation and ferroptosis.
- In vivo, C-Fos depletion suppressed tumor growth and key molecular markers, an effect reversed by SLC7A11 overexpression.
Conclusions
- C-Fos acts as a transcriptional regulator of SLC7A11 in PAAD.
- The C-Fos/SLC7A11 axis promotes PAAD tumor growth by suppressing ferroptosis.
- C-Fos represents a potential therapeutic target for enhancing ferroptosis in pancreatic cancer treatment.
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
Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
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...
Multicellular organisms contain a variety of structurally and functionally distinct cell types, but the DNA in all the cells originated from the same parent cells. The differences in the cells can be attributed to the differential gene expression. Liver cells, whose functions include detoxification of blood, production of bile to metabolize fats, and synthesis of proteins essential for metabolism, must express a specific set of genes to perform their functions. Gene expression also varies with...
Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...