Zvast Biotechnology
Ovarian Cancer
The Mouse SK-OV-3 Model is an internationally recognized gold-standard in vivo model for research on high-grade serous ovarian cancer, recurrent refractory ovarian cancer, HER2-positive ovarian cancer and multi-chemotherapy resistance mechanisms. Derived from human epithelial ovarian serous carcinoma, SK-OV-3 cells exhibit core phenotypes of clinical high-grade ovarian cancer, including malignant hyperproliferation, strong invasion and metastasis potential, significant EMT activation and stable cancer stemness. With inherent high HER2 expression and intrinsic multi-drug resistance to first-line chemotherapies such as cisplatin, carboplatin, paclitaxel and 5-FU, it faithfully recapitulates the refractory pathological characteristics of advanced clinical ovarian cancer, including chemotherapy resistance, tumor microenvironment remodeling, extensive invasion and frequent recurrence. Compared with the ES-2 clear cell carcinoma model, SK-OV-3 better represents the most prevalent serous ovarian cancer subtype in clinical practice, serving as a benchmark cell line for investigating epithelial ovarian cancer stemness regulation, HER2-mediated malignant progression, chemotherapy resistance, EMT invasion and peritoneal implantation metastasis. Logarithmic-phase low-passage SK-OV-3 cells are subcutaneously inoculated into BALB/c-nu immunodeficient nude mice to establish standardized xenograft models with high tumorigenicity, excellent homogeneity, stable malignant phenotypes and constant drug resistance characteristics. This model is widely applied in the exploration of ovarian cancer targeted pathway mechanisms, chemotherapy sensitization, drug resistance reversal, stemness inhibition and combined medication synergism. It fully meets the standardized methodological writing requirements of NSFC projects, postgraduate proposals, dissertations and high-score SCI manuscripts, forming a complete ovarian cancer research system covering both serous and clear cell subtypes together with the ES-2 model.
1. Positive modeling criteria: Clear macroscopic tumor nodules appear 5–7 days after SK-OV-3 cell subcutaneous inoculation. The tumor formation rate is ≥95% within 12 days, and tumor volume ＞50 mm³ is defined as successful modeling. Tumors in the vehicle control group proliferate continuously and stably without spontaneous regression, accurately reproducing the malignant characteristics of rapid proliferation and continuous progression of clinical high-grade serous ovarian cancer.
2. Model reproducibility criteria: The intra-group coefficient of variation (CV) of tumor volume in the vehicle control group is ＜30%, indicating high standardized modeling operation, minimal individual differences and excellent batch stability, fully meeting the quality control requirements of SCI experimental data.
3. Pharmacodynamic response criteria: After intervention with ovarian cancer positive chemotherapy/targeted drugs, the tumor growth inhibition rate (TGI) is ≥35%, and tumor volume and tumor weight are significantly reduced compared with the vehicle control group (P＜0.05). The model has stable and sensitive pharmacodynamic responses to HER2 targeted drugs, chemotherapy sensitizers and stemness inhibitors, suitable for drug screening and mechanism verification of refractory drug-resistant ovarian cancer.
1. HE staining gold standard: Tumor tissues contain a large number of atypical epithelial-derived ovarian cancer cells with large deeply stained nuclei, obvious nucleoli, abundant mitotic figures and disordered and dense cell arrangement, which conform to the typical histological morphological characteristics of human high-grade serous ovarian cancer.
2. Molecular phenotypic criteria: High HER2 protein expression and significantly elevated Ki-67 proliferation index in tumor tissues indicate high proliferation and HER2-driven malignant progression; high expression of SOX2, OCT4 and NANOG stemness markers confirms continuous activation of tumor stemness; low E-cadherin expression and high expression of Vimentin, N-cadherin, MMP2 and MMP9 verify significant EMT activation and strong invasion-metastasis phenotype, perfectly recapitulating the core molecular pathological characteristics of HER2 activation, abnormal stemness, multi-drug resistance and high invasion and recurrence of clinical serous ovarian cancer.
3. Pharmacodynamic response criteria: Compared with the vehicle control group, the treatment group shows down-regulated HER2 expression, significantly reduced stemness markers, decreased Ki-67 proliferation index, increased Cleaved-Caspase-3 apoptosis level and declined expression of EMT and invasion markers, confirming that drugs can target and inhibit HER2 pathway, block tumor stemness, reverse EMT, suppress invasion and metastasis, and reverse chemotherapy resistance.
4. Evidence closed-loop criteria: In vivo histopathological and molecular protein detection results are highly consistent with the in vitro SK-OV-3 cell experimental mechanism trend, forming a complete and credible academic evidence closed-loop.
The Mouse SK-OV-3 Model is an internationally authoritative gold-standard in vivo model for research on high-grade serous ovarian cancer, HER2-positive ovarian cancer, multi-chemotherapy resistance and recurrent metastasis mechanisms. Core academic validity evidence: ① As a classic representative cell line of the most common clinical serous ovarian cancer, SK-OV-3 stably carries four core malignant phenotypes including high HER2 expression, activated tumor stemness, hyperactive EMT and multi-chemotherapy resistance, which are highly consistent with the refractory and recurrent characteristics of clinical advanced ovarian cancer; ② It presents stable in vivo tumorigenesis, typical pathological phenotypes and no batch drift in malignant progression and drug resistance phenotypes with excellent data reproducibility; ③ It has clear gradient pharmacodynamic responses to HER2 targeted therapy, stemness inhibition, chemotherapy sensitization and drug resistance reversal drugs, serving as a core tool model for ovarian cancer translational medical research; ④ It covers multi-dimensional mechanisms including HER2 targeted pathway, tumor stemness, EMT invasion and multi-drug resistance with wide research coverage and in-depth mechanism exploration potential; ⑤ It has been widely accepted by top SCI journals in the field of gynecological oncology for decades. As a benchmark model for basic research, targeted new drug development and drug resistance mechanism exploration of serous ovarian cancer, it complements the ES-2 clear cell model to construct a complete ovarian cancer research system.
The Mouse SK-OV-3 Model is the preferred SCI gold-standard model for research on clinical high-grade serous ovarian cancer, HER2-positive ovarian cancer and multi-drug resistant recurrent ovarian cancer. Core advantages: It perfectly matches the most prevalent clinical serous ovarian cancer subtype, and is more consistent with the pathological characteristics and pathogenesis of mainstream clinical ovarian cancer than clear cell carcinoma models. It inherently possesses four core malignant phenotypes including high HER2 expression, activated tumor stemness, hyperactive EMT invasion and multi-chemotherapy resistance, which highly simulate the refractory characteristics of clinical advanced ovarian cancer such as chemotherapy resistance, rapid progression and frequent recurrence. With stable tumorigenesis, phenotypic homogeneity and extremely low batch error, it has a high data signal-to-noise ratio, suitable for in-depth mechanism exploration of high-score SCI papers and innovative design of NSFC projects. It can carry out multi-dimensional efficacy and mechanism research including targeted therapy, chemotherapy sensitization, drug resistance reversal, stemness inhibition and anti-invasion and metastasis. Complementary with the ES-2 model, it achieves full coverage of the two mainstream ovarian cancer subtypes, greatly improving the systematicness and innovation of research projects with high recognition in fund applications and SCI publications.
The Mouse SK-OV-3 Model is mainly applied to preclinical translational research on HER2 targeted intervention, tumor stemness regulation, EMT invasion and metastasis, multi-chemotherapy resistance reversal and recurrence refractory mechanisms of human high-grade serous ovarian cancer. Core application scenarios: targeted therapy mechanisms and new drug screening for HER2-positive ovarian cancer; analysis of the generation, maintenance and reversal mechanisms of multi-chemotherapy resistance in advanced ovarian cancer; research on the mechanisms of uncontrolled proliferation, invasion, metastasis and recurrence of ovarian cancer mediated by abnormal tumor stemness; in vivo efficacy evaluation of innovative drugs used alone or in combination for chemotherapy sensitization, toxicity reduction, efficacy enhancement and anti-recurrence and metastasis; filling the mechanism research gap of mainstream serous ovarian cancer subtypes, and constructing a complete ovarian cancer research system with the ES-2 clear cell carcinoma model. It fully supports innovative mechanism exploration for NSFC and provincial-level projects, postgraduate proposals, dissertations and high-score SCI papers in gynecological oncology, serving as a core benchmark in vivo model for targeted therapy, drug resistance and stemness research of serous ovarian cancer.
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