Ekspresi protein P53 dan HSP70 pada sel punca karsinoma nasofaring yang resisten terhadap radioterapi

Abstract

Latar belakang: Pada penderita Karsinoma Nasofaring (KNF) masih sering ditemukan kekambuhan meskipun sudah mendapat terapi yang lengkap. Penelitian terbaru membuktikan bahwa kekambuhan disebabkan oleh sel punca KNF yang resisten terhadap radioterapi. Mekanisme resistensi sel punca kanker terhadap radioterapi diduga karena hambatan terhadap apoptosis dan atau memicu proliferasi. Hambatan terhadap apoptosis disebabkan oleh penurunan protein p53 (wild type), selain over-ekspresi
Hsp70. Tujuan: Menjelaskan mekanisme resistensi sel punca KNF terhadap radioterapi berdasarkan profil ekspresi protein p53(wild type)dan Hsp70. Metode: Penelitian true experimental dengan menggunakan rancangan randomisasi kelompok kontrol sebelum dan sesudah tes. Kultur sel punca KNF dibagi menjadi dua kelompok, masing-masing 16 sampel. Pada kelompok perlakuan diberikan paparan radioterapi dengan dosis 1,5 Gy menggunakan pesawat Linac, lalu diinkubasi selama 24 jam. Sebelum dan sesudah perlakuan pada kedua kelompok diperiksa ekspresi p53 (wild type) dan Hsp70. Pemeriksaan menggunakan metode flowcytometry. Hasil: Ekspresi p53 (wild type) antara kelompok perlakuan dan kontrol terdapat
perbedaan yang tidak bermakna dengan p=0,576 (p≥0,05). Ekspresi Hsp70, antara kelompok perlakuan dan kontrol terdapat perbedaan yang tidak bermakna dengan p=0,172 (p≥0,05). Kesimpulan: Tidak terdapat
perubahan ekspresi p53 (wild type) dan Hsp70 pada sel punca KNF yang resisten terhadap radioterapi.

Kata kunci : Sel punca KNF, p53 (wild type), Hsp70, karsinoma nasofaring

ABSTRACT
Background: Recurrences are frequently occurred in nasopharyngeal  carcinoma (NPC) patients, eventhough they had received complete therapy. Recent studies have proved that those recurrences were caused by NPC cancer stem cells that resistant to radiotherapy. Mechanisms of resistance of cancer stem cells to radiotherapy is assumed due to the block of apoptosis and or proliferation inducing. The block of apoptosis was caused by the decrease of p53 (wild type) expression, in addition to Hsp70 over expression. Objective: To find out the mechanism of NPC stem cells that resistant to radiotherapy based on profiles of protein p53 (wild type) and Hsp70 expression. Methods: Using true experimental study by randomized
pre and post test control group design. The cultured NPC stem cells were divided into two groups, with 16 samples each. The treatment group had 1,5Gy dose of radiotherapy exposure with Linac device, then incubated for 24 hours. Both groups were examined for p53 (wild type) and Hsp70 expressions before and after treatment. The examinations were conducted by flowcytometry method. Result: The P53 (wild type) expression between the treatment and control group showed insignificant difference with p=0.576
(p≥0.05). The Hsp70 expression between treatment and control group showed insignificant difference with p=0.172 (p≥0.05). Conclusion: There were no changes of p53 (wild type) and Hsp70 expressions on NPC stem cells that resistant to radiotherapy

Keywords: NPC stem cells, p53 (wild type), Hsp70, nasopharyngeal carcinoma