ارتباط متقابل اتوفاژی و آپوپتوز در پیشرفت بدخیمی هپاتوسلولار کارسینوما

نوع مقاله : مقاله مروری

نویسندگان

1 دانشجوی دکتری بیولوژی تکوینی، مرکز تحقیقات علوم سلولی، پژوهشکده‌ی سلول‌های بنیادی، پژوهشگاه رویان، تهران، ایران

2 دانشجوی دکتری علوم سلولی کاربردی، دانشکده‌ی فن‌آوری‌های نوین پزشکی، جهاد دانشگاهی پژوهشگاه رویان، تهران، ایران

3 دانشجوی دکتری بیوتکنولوژی پزشکی، مرکز تحقیقات علوم سلولی، پژوهشکده‌ی سلول‌های بنیادی، پژوهشگاه رویان، تهران، ایران

4 استادیار، مرکز تحقیقات علوم سلولی، پژوهشکده‌ی سلول‌های بنیادی، پژوهشگاه رویان، تهران، ایران

5 دانشیار، مرکز تحقیقات علوم سلولی، پژوهشکده‌ی سلول‌های بنیادی، پژوهشگاه رویان، تهران، ایران

چکیده

هپاتوسلولار کارسینوما (Hepatocellular carcinoma یا HCC) شایع‌ترین نوع بدخیمی کبد و بر اساس به‌روزرسانی اخیر Globocan در سال 2020، سومین علت مرگ و میر مرتبط با سرطان در جهان است. یکی از اهداف اصلی روش‌‌های درمانی مرسوم این بدخیمی، القای مرگ برنامه‌ریزی شده (آپوپتوز) در سلول‌های توموری است. از جمله مکانیسم‌های مهم تأثیرگذار در پاسخ سلول‌های توموری به آپوپتوز، فرایند اتوفاژی است. اتوفاژی، یک فرایند تخریب وابسته به لیزوزوم حفاظت شده است که به حفظ هموستاز و سازگاری متابولیکی سلول کمک می‌کند. آپوپتوز و اتوفاژی، دو مکانیسم اصلی در تنظیم مرگ و زنده‌مانی سلولی هستند. افزایش اتوفاژی در مراحل مختلف هپاتوسلولار کارسینوما، با افزایش بقای سلول‌های توموری و پیشرفت بدخیمی مرتبط است و از این طریق، فرار سلول‌های سرطانی از آپوپتوز را تسهیل می‌کند. مطالعات متعددی که به بررسی اثر مهار اتوفاژی در القای آپوپتوز سلول‌های توموری هپاتوسلولار کارسینوما پرداخته‌اند، حاکی از افزایش اثرات درمانی القا کننده‌های آپوپتوز پس از مهار اتوفاژی است. این مطالعه، به بررسی ارتباط متقابل اتوفاژی و آپوپتوز در بقای سلول‌های توموری هپاتوسلولار کارسینوما و تغییرات هدفمند تعادل بین این دو فرایند در درمان این بدخیمی پرداخته است.

کلیدواژه‌ها


عنوان مقاله [English]

Autophagy and Apoptosis Crosstalk in Hepatocellular Carcinoma Progression

نویسندگان [English]

  • Homeyra Seydi 1
  • Shukoofeh Torabi 2
  • Roya Ramezankhani 2
  • Bahareh Shokoohian 3
  • Faezeh Shekari 4
  • Massoud Vosough 5
1 PhD Student in Developmental Biology, Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, The Academic Center for Education, Culture and Research (ACECR), Tehran, Iran
2 PhD Student in Applied Cell Sciences, Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, The Academic Center for Education, Culture and Research (ACECR), Tehran, Iran
3 PhD Student in Medical Biotechnology, Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, The Academic Center for Education, Culture and Research (ACECR), Tehran, Iran
4 Assistant professor, Department of Stem Cells and Developmental Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, The Academic Center for Education, Culture and Research (ACECR), Tehran, Iran
5 Associate Professor, Department of Regenerative Medicine, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, The Academic Center for Education, Culture and Research (ACECR), Tehran, Iran
چکیده [English]

Hepatocellular carcinoma (HCC) is the most common type of liver cancer and the third cause of cancer-related death worldwide based on a recent update of Globocan in 2020. The induction of programmed cell death (apoptosis) in tumor cells is one of the main targets of conventional therapies in cancer. One of the key mechanisms that impacts tumor cells apoptotic response is autophagy. Autophagy is a conserved lysosome-dependent degradation process that aids in the maintenance of cell homeostasis and metabolic compatibility. Apoptosis and autophagy are two main processes in controlling cell death and survival. Enhanced autophagy at various stages of HCC is related to increased tumor cells survival and malignancy development, allowing cancer cells to evade apoptosis. Various studies that investigated the effect of autophagy inhibition on apoptosis induction in HCC cells indicated that apoptosis inducers have a stronger therapeutic impact after autophagy inhibition. In this study, the crosstalk between autophagy and apoptosis in cells survival, as well as targeted alterations in the balance between these processes in HCC therapy are investigated.

کلیدواژه‌ها [English]

  • Liver neoplasms
  • Hepatocellular carcinoma
  • Apoptosis
  • Autophagy
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