Zvast Biotechnology
Ovarian Cancer
The Mouse PA-1 Model is a classic international gold-standard in vivo model for research on human teratocarcinoma, malignant germ cell tumors, stem cell carcinogenesis and multistage tumor progression. Derived from human malignant teratoma, PA-1 cells belong to typical embryonic germ cell tumor cell lines with stable stem cell pluripotency, three-germ-layer differentiation potential and activated N-ras proto-oncogene, which can highly simulate the abnormal stemness, disordered multidirectional differentiation and malignant proliferation of clinical germ cell tumors and embryonic tumors. Different from ordinary solid tumor cells, PA-1 retains undifferentiated embryonic stem cell characteristics, can form embryoid bodies in vitro and reconstruct three-germ-layer (ectoderm, mesoderm and endoderm) teratoma structures in vivo. It serves as an exclusive core model for studying malignant transformation of stem cells, tumor stemness maintenance, multistage carcinogenesis progression and pathogenesis of embryonic-origin tumors. Logarithmic-phase low-passage PA-1 cells are subcutaneously inoculated into BALB/c-nu immunodeficient nude mice to achieve nearly 100% stable tumorigenesis with rapid tumor formation, high tumor homogeneity, stable stemness phenotype and negligible batch variation. This model is mainly applied to the research of malignant proliferation, stemness regulation, abnormal three-germ-layer differentiation, N-ras-mediated oncogenic pathways and multistage carcinogenesis of germ cell tumors. It is also suitable for in vivo efficacy evaluation of small-molecule drugs, natural products and nano-formulations targeting cancer stem cells, inhibiting stemness and blocking embryonic tumor progression. With a mature and stable system and high data recognition, it fully meets the methodological writing requirements of NSFC projects, postgraduate proposals, dissertations and SCI manuscripts.
1. Positive modeling criteria: Clear macroscopic tumor nodules appear 4–7 days after PA-1 cell subcutaneous inoculation. The tumor formation rate is ≥98% within 21 days, and tumor volume ＞50 mm³ is defined as successful modeling. Tumors in the vehicle control group proliferate continuously and stably without spontaneous regression, perfectly reproducing the malignant characteristics of high proliferation, high stemness and rapid progression of clinical teratocarcinoma. 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 germ cell tumor positive control drugs, the tumor growth inhibition rate (TGI) is ≥40%, and tumor volume and tumor weight are significantly reduced compared with the vehicle control group (P＜0.05), proving that the model has stable and sensitive pharmacodynamic response to chemotherapeutic drugs and stemness inhibitors, suitable for embryonic tumor drug screening and stemness mechanism verification.
1. HE staining gold standard: Tumor tissues contain a large number of embryonic undifferentiated cells with large deeply stained nuclei and abundant mitotic figures, mixed with diverse differentiated tissues derived from ectoderm, mesoderm and endoderm, forming typical teratoma pathological structures, which are completely consistent with the histological morphological characteristics of human malignant teratoma. 2. Molecular phenotypic criteria: High expression of core stemness markers SOX2, OCT4 and NANOG in tumor tissues confirms continuous activation of tumor stem cell status; widespread positive expression of GFAP (ectoderm), Vimentin (mesoderm) and Desmin (endoderm) verifies the disordered three-germ-layer multidirectional differentiation phenotype; accompanied by abnormal activation of N-ras pathway and high Ki-67 proliferative activity, it perfectly recapitulates the core molecular characteristics of uncontrolled stemness, abnormal differentiation and malignant proliferation of clinical germ cell tumors. 3. Pharmacodynamic response criteria: Compared with the vehicle control group, the treatment group shows significantly down-regulated SOX2/OCT4/NANOG stemness markers, decreased Ki-67 proliferation index, increased Cleaved-Caspase-3 apoptosis level and normalized expression of abnormal three-germ-layer differentiation markers, confirming that drugs can effectively inhibit teratoma stemness, block proliferation, promote apoptosis and correct differentiation disorders. 4. Evidence closed-loop criteria: In vivo histopathological and molecular protein detection results are highly consistent with the in vitro PA-1 cell experimental mechanism trend, forming a complete and credible academic evidence closed-loop.
The Mouse PA-1 Model is a classic and authoritative gold-standard in vivo model for research on human malignant teratoma, germ cell tumors, stem cell carcinogenesis and multistage tumor progression. Core academic validity evidence: ① PA-1 cells possess stable N-ras proto-oncogene activation, embryonic stem cell pluripotency and three-germ-layer differentiation potential, serving as the only classic cell line that can simultaneously simulate malignant transformation of stem cells, differentiation disorders and multistage carcinogenesis; ② It presents an extremely high in vivo tumor formation rate, typical teratoma pathological phenotype and stable stemness phenotype, highly consistent with the embryonic pathogenesis characteristics of clinical germ cell tumors; ③ It is sensitive to stemness inhibitors and germ cell tumor chemotherapeutic drugs with clear pharmacodynamic gradients, suitable for the research and development of anti-cancer stem cell drugs and in-depth mechanism exploration; ④ It covers multi-dimensional mechanisms including stemness regulation, abnormal differentiation, proto-oncogene activation and multistage carcinogenesis with wide research coverage and strong innovation; ⑤ It has been widely accepted by SCI journals in the fields of tumor stem cell research, oncoembryology and multistage carcinogenesis for decades, acting as a benchmark model for basic and translational research of germ cell tumors.
The Mouse PA-1 Model is an irreplaceable SCI gold-standard model for research on cancer stem cells, embryonic-origin tumors and multistage carcinogenesis mechanisms. Core advantages: It uniquely possesses embryonic stem cell pluripotency and three-germ-layer differentiation characteristics, serving as one of the few in vivo models that can simulate the carcinogenic process of malignant transformation and differentiation disorder of stem cells. With inherent N-ras activating mutation, it naturally presents high malignancy, high stemness and high proliferation phenotypes, with nearly 100% tumor formation rate and excellent experimental stability. Different from ordinary epithelial tumor models, it focuses on the unique pathogenesis of embryonic germ cell tumors with unique innovation dimensions and high research blankness. It has stable stemness phenotype and strong specific response to stemness-targeted drugs, acting as the optimal model for screening anti-cancer stem cell drugs and reversing malignant stemness phenotypes. It forms a complementary system with the group’s multi-tumor models, covering multiple carcinogenesis modes of epithelial tumors and embryonic germ tumors with strong systematicness and completeness, enjoying outstanding recognition in NSFC projects and high-score SCI papers.
The Mouse PA-1 Model is mainly used for preclinical mechanism and translational research on human malignant teratoma, germ cell tumors, malignant transformation of stem cells, three-germ-layer differentiation disorder and multistage carcinogenesis. Core application scenarios: mechanism analysis of stemness maintenance and abnormal activation of embryonic tumor stem cells; research on multistage carcinogenesis progression mechanism mediated by N-ras proto-oncogene activation; exploration of the mechanism of three-germ-layer differentiation disorder in tumor malignant progression; in vivo efficacy evaluation of innovative drugs targeting cancer stem cells, inhibiting stemness phenotype and correcting differentiation disorders; research on chemotherapy sensitization and drug resistance reversal of germ cell tumors. It fills the research gap of embryonic tumor pathogenesis that cannot be covered by ordinary epithelial tumor models, fully supporting innovative mechanism exploration of NSFC projects, postgraduate proposals, dissertations and high-score SCI papers in the direction of tumor stem cells, serving as a core benchmark in vivo model for basic and translational research of embryonic germ cell tumors.
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