KORELASI LEVEL EKSPRESI GEN HMGA2 DENGAN DISTRIBUSI DAN INTENSITAS PROTEIN HMGA2 PADA KANKER SERVIKS
Abstract
Pendahuluan: Kanker serviks yang merupakan penyebab utama kematian wanita terkait kanker, dengan infeksi Human Papillomavirus (HPV) tipe 16 dan 18 sebagai faktor risiko utama. Keterlambatan diagnosis dan kurangnya program skrining yang efektif menyebabkan sebagian besar kasus kanker serviks baru terdeteksi pada stadium lanjut, sehingga sulit ditangani secara efektif. Gen HMGA2, yang berperan penting dalam karsinogenesis, telah diteliti sebagai salah satu faktor yang berpotensi menjadi biomarker dalam deteksi dini dan penilaian perkembangan kanker serviks. Oleh karena itu, penelitian ini berfokus pada pengukuran ekspresi gen HMGA2 serta distribusi dan intensitas ekspresinya pada jaringan kanker serviks. Penelitian ini bertujuan untuk mengeksplorasi korelasi antara ekspresi gen HMGA2 dengan distribusi dan intensitas ekspresinya pada jaringan kanker serviks. Metode: penelitian ini menggunakan metode eksperimental laboratorium dengan menganalisis ekspresi gen HMGA2 melalui teknik qPCR dan distribusi serta intensitas protein HMGA2 menggunakan imunohistokimia (IHC). Sampel yang digunakan dalam penelitian ini adalah hasil biopsi jaringan kanker serviks yang telah dikonfirmasi secara histopatologi. Hasil: Berdasarkan data demografi sampel penelitian, karakteristik usia responden menunjukkan bahwa sebagian besar sampel berada dalam rentang usia 45–59 tahun (60%), diikuti oleh kelompok usia di atas 60 tahun (30%), dan kelompok usia 19–44 tahun sebagai yang paling sedikit (10%). Walaupun secara kuantatif tidak berbeda signifikan (p>0,05), namun secara kualitatif, distribusi dan intensitas ekspresi HMGA2 memiliki perbedaan. Terdapat korelasi positif kuat dan signifikan antara ekspresi mRNA HMGA2 dengan intensitas ekspresi protein HMGA2 pada jaringan kanker serviks (r = 0,8175; p = 0,0247). Demikian halnya dengan ekspresi mRNA HMGA2 yang memiliki korelasi positif kuat dengan distribusi area ekspresi protein HMGA2 (r = 0,6684; p = 0,1007), namun tidak signifikan. Kesimpulan: Terdapat korelasi positif yang kuat antara ekspresi mRNA HMGA2 dengan intensitas dan distribusi protein HMGA2, walaupun tidak ditemukan korelasi yang signifikan pada distribusi protein HMGA2.
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References
Gao, G., & Smith, D. I. (2017). Human papillomavirus and the development of different cancers. Cytogenetic and Genome Research, 150(3-4), 185–193. https://doi.org/10.1159/000458166
Gao, X., Dai, M., Li, Q., et al. (2017). HMGA2 regulates lung cancer proliferation and metastasis. Thoracic Cancer, 8(5), 501–510. https://doi.org/10.1111/1759-7714.12476
Gao, Y., Ma, J., Gao, F., et al. (2013). The evaluation of older patients with cervical cancer. Clinical Interventions in Aging, 8, 783–788. https://doi.org/10.2147/CIA.S45613
Hartanti, M. D., Dwi, E., Rachmadhany, A., Tazkiatul, I., Mustopa, I., Syaputra, E., et al. (2020). High mobility group at-hook expression is elevated in cervical cancer. International Journal of Pharmaceutical Research, 4, 2332–2338. https://doi.org/10.31838/ijpr/2020.12.04.322
Hu, Z., Zhu, D., Wang, W., Li, W., Jia, W., Zeng, X., et al. (2015). Genome-wide profiling of HPV integration in cervical cancer identifies clustered genomic hot spots and a potential microhomology-mediated integration mechanism. Nature Genetics, 47(2), 158–163. https://doi.org/10.1038/ng.3178
Li, M. Y., Liu, J. Q., Chen, D. P., et al. (2017). Radiotherapy induces cell cycle arrest and cell apoptosis in nasopharyngeal carcinoma via the ATM and Smad pathways. Cancer Biology & Therapy, 18(9), 681–693. https://doi.org/10.1080/15384047.2017.1360442
Ma Q, Ye S, Liu H, Zhao Y, Mao Y, Zhang W. HMGA2 promotes cancer metastasis by regulating epithelial-mesenchymal transition. Front Oncol. 2024 Feb 1;14:1320887. doi: 10.3389/fonc.2024.1320887. PMID: 38361784; PMCID: PMC10867147.
Mansoori, B., Mohammadi, A., Ditzel, H. J., Duijf, P. H. G., Khaze, V., Gjerstorff, M. F., et al. (2021). HMGA2 as a critical regulator in cancer development. Genes, 12(2), 269. https://doi.org/10.3390/genes12020269
Maruyama T, Saito K, Higurashi M, Ishikawa F, Kohno Y, Mori K, Shibanuma M. HMGA2 drives the IGFBP1/AKT pathway to counteract the increase in P27KIP1 protein levels in mtDNA/RNA-less cancer cells. Cancer Sci. 2023 Jan;114(1):152-163. doi: 10.1111/cas.15582. Epub 2022 Sep 26. PMID: 36102493; PMCID: PMC9807519.
Mehrdad Hashemi, Mohsen Rashidi, Kiavash Hushmandi, Timo L.M. ten Hagen, Shokooh Salimimoghadam, Afshin Taheriazam, Maliheh Entezari, Mojtaba Falahati, HMGA2 regulation by miRNAs in cancer: Affecting cancer hallmarks and therapy response, Pharmacological Research,Volume 190, 2023, 106732, https://doi.org/10.1016/j.phrs.2023.106732.
Sreedevi, A., Javed, R., & Dinesh, A. (2015). Epidemiology of cervical cancer with special focus on India. International Journal of Women's Health, 7, 405–414. https://doi.org/ 10.2147/IJWH.S50001
Sung, H., Ferlay, J., Siegel, R. L., Laversanne, M., Soerjomataram, I., Jemal, A., et al. (2021). Global cancer statistics 2020: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA: A Cancer Journal for Clinicians, 71(3), 209–249. https://doi.org/10.3322/caac.21660
Walker, S., & Hamilton, W. (2017). Risk of cervical cancer in symptomatic women aged ≥40 in primary care: A case-control study using electronic records. European Journal of Cancer Care, 26(3), e12706. https://doi.org/10.1111/ecc.12706
World Health Organization. (2022). Cervical cancer. WHO. Retrieved May 11, 2022, from https://www.who.int/news-room/fact-sheets/detail/cervical-canc

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