Context dependent isoform specific PI3K inhibition confers drug resistance in hepatocellular carcinoma cells.

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Narci K., Kahraman D. C., Koyas A., Ersahin T., Tuncbag N., Atalay R. C.

BMC cancer, cilt.22, sa.1, ss.320, 2022 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 22 Sayı: 1
  • Basım Tarihi: 2022
  • Doi Numarası: 10.1186/s12885-022-09357-y
  • Dergi Adı: BMC cancer
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, CAB Abstracts, CINAHL, EMBASE, MEDLINE, Veterinary Science Database, Directory of Open Access Journals
  • Sayfa Sayıları: ss.320
  • Anahtar Kelimeler: Liver Cancer, PI3K, Akt, mTOR pathway, Network analysis, Synergy, Resistance, SIGNALING PATHWAYS, PROLIFERATION, SORAFENIB, PROTEIN, OBESITY, GENES
  • Orta Doğu Teknik Üniversitesi Adresli: Evet

Özet

Background: Targeted therapies for Primary liver cancer (HCC) is limited to the multi-kinase inhibitors, and not fully effective due to the resistance to these agents because of the heterogeneous molecular nature of HCC developed during chronic liver disease stages and cirrhosis. Although combinatorial therapy can increase the efficiency of targeted therapies through synergistic activities, isoform specific effects of the inhibitors are usually ignored. This study concentrated on PI3K/Akt/mTOR pathway and the differential combinatory bioactivities of isoform specific PI3K-alpha inhibitor (PIK-75) or PI3K-beta inhibitor (TGX-221) with Sorafenib dependent on PTEN context.