Publications by authors named "Rushaniya Fazliyeva"

Rapidly proliferating cancer cells have a greater requirement for cholesterol than normal cells. Tumor cells are largely dependent on exogenous lipids given that their growth requirements are not fully met by endogenous pathways. Our current study shows that ccRCC cells have redundant mechanisms of cholesterol acquisition.

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Since the early 1940s, androgen ablation has been the cornerstone of treatment for prostate cancer (PC). Importantly, androgen receptor (AR) signaling is vital not only for the initiation of PC, which is initially androgen-dependent, but also for castration-resistant disease. Recent studies demonstrated clear promise of the poly(ADP-ribose) polymerase 1 (PARP-1) inhibitors for targeting prostate cancer cells harboring mutations in DNA damage-repair genes.

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Article Synopsis
  • Prostate cancer (PC) treatment typically involves androgen deprivation therapy followed by androgen receptor signaling inhibitors, but most patients develop resistance within two years.
  • Acetyl-coenzyme A (acetyl-CoA) is crucial for cancer metabolism and can enhance androgen receptor activity through acetylation and increasing related gene expression.
  • Research shows that PC cells adapt to AR signaling inhibitors by boosting the enzyme ATP-citrate lyase, which increases acetyl-CoA levels, and inhibiting this enzyme can suppress androgen receptor activation.
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Background: The RNA-binding protein Musashi-2 (MSI2) controls the translation of proteins that support stem cell identity and lineage determination and is associated with progression in some cancers. We assessed MSI2 as potential clinical biomarker in colorectal cancer (CRC) and tubulovillous adenoma (TA) of colon mucosa.

Methods: We assessed 125 patients, of whom 20 had polyps of the colon (TAs), and 105 had CRC.

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Article Synopsis
  • * Researchers found that when MSI2 is removed, it lowers the levels of another protein called EGFR, which is important for cancer cell growth.
  • * Depleting MSI2 makes NSCLC cells, especially those with changes in EGFR, less able to grow and makes treatments that target EGFR more effective.
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Background: Multi-targeted tyrosine kinase inhibitors (TKIs) are the standard of care for patients with advanced clear cell renal cell carcinoma (ccRCC). However, a significant number of ccRCC patients are primarily refractory to targeted therapeutics, showing neither disease stabilisation nor clinical benefits.

Methods: We used CRISPR/Cas9-based high-throughput loss of function (LOF) screening to identify cellular factors involved in the resistance to sunitinib.

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Tissue-specific loss-of-function (LOF) analysis is essential for characterizing gene function. Here, we present a simple, yet highly efficient, clustered regularly interspaced short palindromic repeats (CRISPR)-mediated tissue-restricted mutagenesis (CRISPR-TRiM) method for ablating gene function in This binary system consists of a tissue-specific Cas9 and a ubiquitously expressed multi-guide RNA (gRNA) transgene. We describe convenient toolkits for making enhancer-driven Cas9 lines and multi-gRNAs that are optimized for mutagenizing somatic cells.

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