Publications by authors named "C Babra Waryah"
Cellular plasticity in cancer enables adaptation to selective pressures and stress imposed by the tumor microenvironment. This plasticity facilitates the remodeling of cancer cell phenotype and function (such as tumor stemness, metastasis, chemo/radio resistance), and the reprogramming of the surrounding tumor microenvironment to enable immune evasion. Epithelial plasticity is one form of cellular plasticity, which is intrinsically linked with epithelial-mesenchymal transition (EMT).
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- Epithelial-mesenchymal transition (EMT) is a reversible process that cancer cells use to promote tumor growth, with the transcription factor ZEB1 playing a crucial role in this progression, particularly in aggressive triple negative breast cancers (TNBCs).
- Researchers used a CRISPR/dCas9 approach to silence ZEB1 in TNBC models, leading to significant tumor suppression and unveiling a set of 26 genes linked to ZEB1 that contribute to an epigenetic shift toward a more epithelial state.
- The study highlights how the changes in the epigenome resulting from ZEB1 silencing can be utilized for innovative therapeutic strategies in precision oncology, offering hope for better outcomes in challenging breast cancer cases.
Article Synopsis
- Epigenetic silencing of tumor suppressor genes (TSGs) plays a significant role in the development of hepatocellular carcinoma (HCC), and using CRISPR-activation (CRISPRa) can help reverse this process by targeting these genes directly.
- Analysis of HCC data identified 12 potential TSGs that are silenced due to DNA methylation, and all samples tested had at least one silenced TSG, indicating that a targeted treatment approach could improve patient outcomes.
- The study demonstrates that using a CRISPRa system to reactivate specific TSGs in HCC cells can successfully inhibit cancer-related processes like cell growth and movement, highlighting its potential for personalized therapies.
Adipogenesis associated Mth938 domain containing (AAMDC) represents an uncharacterized oncogene amplified in aggressive estrogen receptor-positive breast cancers. We uncover that AAMDC regulates the expression of several metabolic enzymes involved in the one-carbon folate and methionine cycles, and lipid metabolism. We show that AAMDC controls PI3K-AKT-mTOR signaling, regulating the translation of ATF4 and MYC and modulating the transcriptional activity of AAMDC-dependent promoters.
View Article and Find Full Text PDFAberrant gene expression is a hallmark of cancer. Although transcription is traditionally considered 'undruggable', the development of CRISPR-associated protein 9 (Cas9) systems offers enormous potential to rectify cancer-associated transcriptional abnormalities in malignant cells. However delivery of this technology presents a critical challenge to overcome in order to realize clinical translation for cancer therapy.
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