Cisplatin has been used for decades for the treatment of ovarian cancer. However, despite its potent anticancer effect, cisplatin’s efficacy as a single agent was inadequate in patients with advanced stage. Curcumin has been shown to sensitize cisplatin activity in several cancer models. However, the low bioavailability of curcumin has limited its anticancer potential. Hence, nano-formulation of curcumin was developed to increase its therapeutic efficacy in ovarian cancer. The objective of this study was to investigate the mechanism of curcumin nanoparticles given in combination with cisplatin in rat ovarian carcinoma induced by dimethylbenz(a)anthracene (DMBA). The administration of cisplatin and nanocurcumin resulted in a significant reduction in ovarian tumor volume and weight. Furthermore, there were reduction in expressions of Ki67, TGF-β, PI3K, and Akt phosphorylation. Co-treatment of cisplatin and nanocurcumin also reduced JAK expression, STAT3 phosphorylation, and reduced IL-6 concentrations. Altogether, nanocurcumin, given as a co-treatment with cisplatin has therapeutic potential in ovarian cancer models by inhibiting proliferation through downregulation of PI3K/Akt and JAK/STAT3 signaling pathways.
Background: Ovarian carcinoma is one of the most deadly malignancies in the gynecologic field. The cause is not yet known, and the clinical symptoms are not specific. Endometrioid carcinoma and ovarian clear cell carcinoma can originate from endometriosis and are known as endometriosis-related ovarian carcinoma (EAOC). Development of EAOC experimental animal models is needed for basic research and clinical preparation of human tissue tests. This study aimed to determine the role of the ARID1A gene mutation in the carcinogenetic process of EAOC in experimental animal models induced with DMBA. Methods: In this study, the EAOC experimental model was developed using the autoimplantation technique and DMBA induction. This study involved placebo surgery mice (sham), endometrial autoimplantation, and a combination of endometrial autoimplantation and DMBA induction, which were sacrificed at weeks 5, 10, and 20, respectively. Histopathological assessment and immunohistochemical ARID1A staining with an assessment of positive percentages were carried out on 200 cells. Results: This study produced 1 (20%) atypical endometriosis and 1 (20%) clear cell carcinoma at implantation and after 10 weeks of DMBA induction, and 100% endometrioid carcinoma in the DMBA-induced group. ARID1A staining did not show any significant difference (p = 0.313) in all groups. Conclusion: The combination of endometrial autoimplantation techniques and DMBA induction in the ovary produced atypical endometriosis, clear cell carcinoma, and endometrioid carcinoma, where time is an important factor. There was no significant difference in ARID1A expression between the treatment and control groups.
Tujuan penelitian ini adalah untuk meneliti aktivitas antikanker ekstrak etanol 70 % daging buah Mahkota dewa (Phaleria macrocarpa (Scheff.) Boerl.) dengan menggunakan tumor payudara mencit C3H yang diinduksi dengan cara transplantasi. Tigapuluh dua mencit C3H dibagi secara acak menjadi 4 kelompok, yaitu 1 kelompok kontrol dan 3 kelompok yang mendapat ekstrak etanol daging buah Mahkota dewa masing-masing 20,40, dan 80 kali dosis manusia, diberikan secara oral melalui sonde lambung runtuk selama 30 hari, setelah transplantasi tumor. Berat mencit dan volume tumor diukur dua kali seminggu. Berat tumor ditimbang setelah hewan coba dimatikan (menggunakan eter), lalu difiksasi dengan formaldehid untuk pembuatan preparat histopatologis. Aktivitas proliferasi sel tumor dinilai dengan menghitung butir AgNOR setelah pewarnaan dengan perak nitrat koloidal. Apoptosis dinilai dengan pewarnaan Tunel, dan luas daerah nekrosis dinilai dengan pewarnaan hematoksilin eosin. Hasil penelitian ini memperlihatkan bahwa tidak ada perbedaan bermakna dalam volume tumor, berat tumor, nilai AgNOR, dan luas daerah nekrosis antara kelompok kontrol dan ketiga kelompok yang mendapat ekstrak etanol daging buah Mahkota dewa (p>0,05), tetapi indeks apoptosis meningkat secara bermakna pada kelompok D3 (ekstrak Mahkota dewa 80 kali dosis manusia) (p<0,05). Dari penelitian ini disimpulkan bahwa ekstrak etanol daging buah Mahkota dewa 20,40,dan 80 kali dosis manusia, yang diberikan secara oral setelah transplantasi tumor untuk selama 30 hari, tidak menghambat pertumbuhan tumor payudara mencit C3H yang diinduksi dengan cara transplantasi, tetapi apoptosis meningkat pada kelompok yang mendapat ekstrak etanol daging buah Mahkota dewa 80 kali dosis manusia.
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