Lipid metabolism associated PLPP4 gene drives oncogenic and adipogenic potential in breast cancer cells
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.This study identifies Phospholipid Phosphatase 4 (PLPP4) as an oncogene driving breast cancer progression by promoting lipid metabolism and adipogenic activity. Downregulating PLPP4 reduces cancer cell growth and lipid accumulation.
Area Of Science
- Oncology
- Molecular Biology
- Cancer Metabolism
Background
- Lipid metabolic reprogramming is crucial for cancer growth, metastasis, and therapy resistance.
- Adipocytes and adipocyte-like cells fuel cancer cells, enhancing their oncogenic potential.
Purpose Of The Study
- Identify dysregulated lipid metabolism genes in breast cancer.
- Uncover the role of an unexplored gene in cancer potential.
Main Methods
- Cancer database analysis to identify seven seed signature genes.
- Experimental validation of PLPP4 in breast cancer cell lines (MDA-MB 231, MCF-7) using knockdown and overexpression.
- Analysis of lipid droplets, triacylglycerol (TAG) formation, glycerol release, and adipogenic markers.
Main Results
- Seven key genes including PLPP4 were identified through database analysis.
- PLPP4 was confirmed as an oncogene, regulating triacylglycerol metabolism.
- PLPP4 overexpression increased lipid accumulation and adipogenic markers; PLPP4 downregulation reversed these effects.
- BMP2-induced adipogenic potential was mitigated by PLPP4 downregulation.
Conclusions
- PLPP4 acts as an oncogene in breast cancer, likely by modulating adipogenic activity.
- BMP2 signaling drives PLPP4 to enhance both oncogenic and adipogenic potential in breast cancer cells.
- This study reveals PLPP4 as a novel target for therapeutic intervention in breast cancer.
Contact us if these videos are not relevant.
Contact us if these videos are not relevant.
Related Concept Videos
Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...
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...