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مرکز تحقیقات غدد و متابولیسم

دانشگاه علوم پزشکی تهران

  • تاریخ انتشار : 1402/06/06 - 12:07
  • : 83
  • زمان مطالعه : 1 دقیقه

thyroid cancer

The effects of Abemaciclib on cell cycle and apoptosis regulation in anaplastic thyroid cancer cells

Anaplastic thyroid cancer (ATC) is an aggressive subtype of thyroid cancer, accounting for 1 to 2% of all cases. Deregulations of cell cycle regulatory genes including cyclins, cyclin-dependent kinases (CDKs), and endogenous inhibitors of CDKs (CKIs) are hallmarks of cancer cells and hence, studies indicate the inhibition of CDK4/6 kinases and cell cycle progression as potent therapeutic strategies. In this study, we investigated the anti-tumor activity of Abemaciclib, a CDK4 and CDK6 inhibitor, in ATC cell lines

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Anaplastic thyroid cancer (ATC) is an aggressive subtype of thyroid cancer, accounting for 1 to 2% of all cases. Deregulations of cell cycle regulatory genes including cyclins, cyclin-dependent kinases (CDKs), and endogenous inhibitors of CDKs (CKIs) are hallmarks of cancer cells and hence, studies indicate the inhibition of CDK4/6 kinases and cell cycle progression as potent therapeutic strategies. In this study, we investigated the anti-tumor activity of Abemaciclib, a CDK4 and CDK6 inhibitor, in ATC cell lines.

The ATC cell lines C643 and SW1736 were selected to study the antiproliferative effects of Abemaciclib using a cell proliferation assay and crystal violet staining assay. Annexin V/PI staining and cell cycle analysis by flow cytometry were also performed to examine the effects on apoptosis induction and cell cycle arrest. Wound healing assay and zymography analysis examined the effects of the drug on invasive abilities of ATC cells and Western blot analyses were applied to further study the anti-tumor mechanism of Abemaciclib, in addition to combination treatment with alpelisib. Our data demonstrated that Abemaciclib significantly inhibited cell proliferation and increased cellular apoptosis and cell cycle arrest in ATC cell lines, while considerably reducing cell migration and colony formation. The mechanism seemed to involve the PI3K pathway.

Our preclinical data highlight CDK4/6 as interesting therapeutic targets in ATC and suggest CDK4/6-blockade therapies as promising strategies in this malignancy.

 

  • Article_DOI : DOI:10.1007/s11033-023-08255-1
  • نویسندگان : elaheh s abutorabi,sahar shamsaiegahkani , seied a mousavi,arash poursheikhani,vahid haghpanah , davood bashash, majid momeny, seyed h ghaffari, bahareh kashani, arash poursheikhani
  • گروه خبر : مقالات علمی,انگلیسی ,مقالات
  • کد خبر : 245039
کلمات کلیدی
فاطمه  ذاکرحسینی
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فاطمه ذاکرحسینی

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