Zvast Biotechnology
Ovarian Cancer
The Mouse ES-2 Model is the most classic and highly recognized gold-standard in vivo model for human ovarian clear cell carcinoma (OCCC) research. Derived from human ovarian clear cell carcinoma, ES-2 cells are characterized by high invasiveness, strong metastasis potential and primary chemotherapy resistance. Compared with ovarian serous carcinoma cells, ES-2 cells exhibit vigorous proliferative activity, high in vivo tumorigenicity, prominent abdominal metastasis tendency and cisplatin tolerance, which faithfully recapitulate the typical clinical pathological features of ovarian clear cell carcinoma, including malignant progression, early invasion and metastasis, chemotherapy resistance and poor recurrent prognosis. With stable malignant phenotypes, negligible batch variation and high in vivo proliferation homogeneity, ES-2 serves as a benchmark cell model for exploring ovarian cancer proliferation and invasion, microenvironment remodeling, EMT malignant transformation, chemotherapy resistance reversal and targeted drug screening. Logarithmic-phase low-passage human ES-2 ovarian clear cell carcinoma cells are subcutaneously inoculated into BALB/c-nu immunodeficient nude mice to establish subcutaneous solid tumor xenograft models with stable tumorigenesis, high phenotypic fidelity and excellent data reproducibility. This model is widely applied in preclinical pharmacodynamic evaluation of malignant progression mechanisms, targeted pathway regulation, chemotherapy sensitization, drug resistance reversal and novel anti-tumor drugs for ovarian clear cell carcinoma, fully meeting the standardized methodological writing requirements of NSFC projects, postgraduate proposals, dissertations and high-score SCI manuscripts.
1. Positive modeling criteria: Clear subcutaneous tumor nodules appear 4–6 days after ES-2 cell inoculation. The tumor take rate is ≥95% within 10 days, and tumor volume ＞50 mm³ is defined as successful modeling. Tumors in the vehicle control group grow rapidly and continuously without spontaneous regression, which is completely consistent with the high-proliferation and high-malignant progression characteristics of clinical ovarian clear cell carcinoma.
2. Reproducibility criteria: The intra‑group coefficient of variation (CV) of tumor volume in the vehicle group is ＜30%, indicating good modeling uniformity and low systematic error, which strictly meets SCI quality control requirements for data repeatability.
3. Pharmacodynamic response criteria: First-line ovarian cancer positive drug intervention achieves TGI≥40% with significantly reduced tumor volume and weight compared with the control group (P＜0.05). The model presents stable and sensitive responses to chemotherapeutic drugs and targeted inhibitors, enabling accurate evaluation of chemotherapy sensitization, invasion blocking and drug resistance reversal effects in ovarian cancer.
1. HE gold standard: Tumor tissues consist of a large number of atypical ovarian clear cells with large cell volume, transparent cytoplasm, large deeply stained nuclei, abundant mitotic figures and disordered cell arrangement, which conform to the typical pathological morphological characteristics of human ovarian clear cell carcinoma.
2. Molecular phenotypic criteria: High Ki‑67 expression in tumor tissues indicates strong proliferative activity; high expression of Vimentin, N-cadherin, MMP2 and MMP9 combined with low E‑cadherin expression confirms significant EMT activation and high invasion-metastasis phenotype, perfectly recapitulating the core molecular characteristics of malignant progression, high invasiveness and primary drug resistance of clinical ovarian clear cell carcinoma.
3. Pharmacodynamic response criteria: Treatment groups show down-regulated Ki‑67 expression, up-regulated Cleaved‑Caspase‑3, recovered E‑cadherin and reduced expression of Vimentin/N-cadherin/MMP2/MMP9, confirming that drugs can effectively inhibit ovarian cancer proliferation, promote apoptosis, reverse EMT, block invasion and metastasis, and reverse chemotherapy resistance.
4. Evidence closed‑loop criteria: In vivo tissue detection results are highly consistent with in vitro ES-2 cell mechanistic experiments, forming a complete and credible evidence chain of targeted intervention mechanisms.
The Mouse ES-2 Model is an internationally recognized gold-standard in vivo model for research on malignant progression, invasion and metastasis, EMT transformation and chemotherapy resistance of human ovarian clear cell carcinoma. Core validity evidence: ① As the most classic exclusive cell line for ovarian clear cell carcinoma, ES-2 cells stably retain the malignant phenotypes of high invasion, high metastasis and chemotherapy resistance of clinical ovarian cancer; ② It presents high in vivo tumor formation rate, typical tumor pathological phenotype and stable malignant progression, accurately simulating the pathological characteristics of primary drug resistance, early invasion and rapid progression of clinical ovarian clear cell carcinoma; ③ It has clear gradient pharmacodynamic responses to chemotherapy sensitizers, targeted anti-invasion drugs and drug resistance reversal drugs, suitable for translational medical research of ovarian cancer; ④ It covers multi-dimensional mechanisms including proliferation and apoptosis, EMT malignant transformation, stromal invasion and chemotherapy resistance with wide research coverage and in-depth mechanism exploration potential; ⑤ It has been widely accepted by SCI journals in the field of gynecological oncology for decades. As a core benchmark model for basic and translational research of ovarian clear cell carcinoma, it is applicable for methodology construction of various projects, research proposals and high-score papers.
The Mouse ES-2 Model is an exclusive SCI gold-standard model for targeted therapy, chemotherapy sensitization, invasion-metastasis and drug resistance mechanism research of ovarian clear cell carcinoma. Core advantages: As the only highly stable in vivo model for ovarian clear cell carcinoma, it specifically matches the clinically rare but highly malignant, drug-resistant and recurrent ovarian clear cell carcinoma subtype, making up for the research defects of ordinary serous ovarian cancer models. It features stable in vivo tumorigenesis, homogeneous proliferation and minimal batch variation with high signal-to-noise ratio and strong data reproducibility, suitable for in-depth mechanism exploration of high-score papers and innovative design of NSFC projects. It inherently possesses high EMT activation, strong invasion-metastasis and primary chemotherapy resistance phenotypes, perfectly simulating the refractory clinical characteristics of ovarian cancer. It can accurately carry out multi-dimensional mechanism research including ovarian cancer malignant progression, invasion-metastasis blockage, EMT reversal, chemotherapy sensitization and drug resistance reversal. It forms a complete complementary system with the group’s multi-tumor models, covering gynecological tumors, gastrointestinal tumors, urinary tumors and reproductive tumors with strong systematicness and outstanding innovation, enjoying excellent recognition in SCI manuscripts and fund applications.
The Mouse ES-2 Model is mainly applied to preclinical mechanism and translational research on malignant proliferation, EMT invasion and metastasis, chemotherapy resistance and targeted sensitization of human ovarian clear cell carcinoma. Core application scenarios: analysis of unique malignant progression and high drug resistance mechanisms of ovarian clear cell carcinoma; research on invasion, metastasis and recurrence mechanisms mediated by tumor EMT activation; in-vivo efficacy evaluation of innovative drugs targeting inhibition of ovarian cancer proliferation, blockage of stromal invasion and reversal of EMT malignant phenotypes; exploration of synergistic efficacy and detoxification mechanisms of chemotherapy sensitization, drug resistance reversal and combined medication for ovarian cancer. It fills the research gap of clear cell subtype that cannot be covered by serous ovarian cancer models, fully supports innovative mechanism exploration for NSFC and provincial-level projects, postgraduate proposals, dissertations and high-score SCI papers in gynecological oncology, serving as an indispensable core gold-standard in-vivo model for basic and targeted translational research of ovarian clear cell carcinoma.
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