SCC145
ID8 Mouse Ovarian Surface Epithelial Cell Line
Mouse
Synonym(s):
ID-8, ID8/MOSEC
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All Photos(2)
About This Item
UNSPSC Code:
41106514
eCl@ss:
32011203
NACRES:
NA.81
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product name
ID8 Mouse Ovarian Surface Epithelial Cell Line, ID8 mouse ovarian surface epithelial cell line is frequently used as a syngeneic mouse model for human ovarian cancer.
biological source
mouse
technique(s)
cell culture | mammalian: suitable
shipped in
liquid nitrogen
General description
ID8 is one of 10 clonal lines established from late passaged C57BL/6 murine ovarian surface epithelial cells (MOSEC) . Intraperitoneal injection of each of the 10 clonal lines into C57BL/6 mice resulted in formation of peritoneal tumors and ascitic fluid. Of the 10 clonal lines, ID8 exhibited the highest tumor load. ID8 cell line is a highly published and well characterized cell line and is frequently used as a syngeneic mouse model for ovarian cancer.
Ovarian cancer is the fourth leading cause of cancer-related deaths in women. The disease is frequently diagnosed at later stages, with tumors detected throughout the peritoneal cavity. Approximately 90% of ovarian tumors arise from ovarian surface epithelial cells . Human and mouse ovarian surface epithelial cells (OSE) have been isolated and are used to develop ovarian cancer models. These models typically involve injection of the human/mouse OSE cells subcutaneously, intraperitoneally or orthotopically into immune deficient mice. A common drawback to these models is the absence of an intact immune system in the host mice.
In 2000, an immune-competent syngeneic mouse model for ovarian cancer was reported . Mouse ovarian surface epithelial cells (MOSEC) isolated from C57BL/6 mice were found to spontaneously transform into malignant tumorigenic cells following prolonged passages in vitro . Late passage MOSEC lost the classical “cobblestone” contact-inhibited in vitro properties reminiscent of normal epithelial cells and instead grew as multi-layered cell clusters indicative of transformed cells. Intraperitoneal injection of late passaged MOSEC into athymic and normal, immune-intact, syngeneic C57BL/6 mice gave rise to tumors throughout the abdominal cavity like those observed in women with Stage III and IV cancer . MOSEC are thus useful syngeneic mouse models to study the role of the immune system in the establishment and progression of ovarian cancer.
In 2000, an immune-competent syngeneic mouse model for ovarian cancer was reported . Mouse ovarian surface epithelial cells (MOSEC) isolated from C57BL/6 mice were found to spontaneously transform into malignant tumorigenic cells following prolonged passages in vitro . Late passage MOSEC lost the classical “cobblestone” contact-inhibited in vitro properties reminiscent of normal epithelial cells and instead grew as multi-layered cell clusters indicative of transformed cells. Intraperitoneal injection of late passaged MOSEC into athymic and normal, immune-intact, syngeneic C57BL/6 mice gave rise to tumors throughout the abdominal cavity like those observed in women with Stage III and IV cancer . MOSEC are thus useful syngeneic mouse models to study the role of the immune system in the establishment and progression of ovarian cancer.
Quality
• Each vial contains ≥ 1X106 viable cells.
• Cells are tested negative for infectious diseases by a Mouse Essential CLEAR panel by Charles River Animal Diagnostic Services.
• Cells are verified to be of mouse origin and negative for inter-species contamination from rat, chinese hamster, Golden Syrian hamster, human and non-human primate (NHP) as assessed by a Contamination CLEAR panel by Charles River Animal Diagnostic Services.
• Cells are negative for mycoplasma contamination
• Cells are tested negative for infectious diseases by a Mouse Essential CLEAR panel by Charles River Animal Diagnostic Services.
• Cells are verified to be of mouse origin and negative for inter-species contamination from rat, chinese hamster, Golden Syrian hamster, human and non-human primate (NHP) as assessed by a Contamination CLEAR panel by Charles River Animal Diagnostic Services.
• Cells are negative for mycoplasma contamination
Other Notes
This product is intended for sale and sold solely to academic institutions for internal academic research use per the terms of the "Academic Use Agreement" as detailed in the product documentation. For information regarding any other use, please contact licensing@emdmillipore.com.
Storage Class Code
12 - Non Combustible Liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
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Zixiang Wang et al.
Nature communications, 13(1), 6246-6246 (2022-10-22)
Dysregulated expression of splicing factors has important roles in cancer development and progression. However, it remains a challenge to identify the cancer-specific splicing variants. Here we demonstrate that spliceosome component BUD31 is increased in ovarian cancer, and its higher expression
Li Jiang et al.
Frontiers in immunology, 9, 2927-2927 (2019-01-09)
Fatty acid synthase (FASN), the key metabolic enzyme of de novo lipogenesis, provides proliferative and metastatic capacity directly to cancer cells have been described. However, the impact of aberrant activation of this lipogenic enzyme on host anti-tumor immune milieu remains
Dhanir Tailor et al.
iScience, 26(11), 108292-108292 (2023-11-29)
Guanylate-binding protein 1 (GBP1) is known as an interferon-γ-induced GTPase. Here, we used genetically modified ovarian cancer (OC) cells to study the role of GBP1. The data generated show that GBP1 inhibition constrains the clonogenic potential of cancer cells. In vivo
K F Roby et al.
Carcinogenesis, 21(4), 585-591 (2000-04-07)
Mouse ovarian surface epithelial cells (MOSEC) were obtained from virgin, mature mice by mild trypsinization and were repeatedly passaged in vitro. Early passage cells (<20 passages) exhibited a cobblestone morphology and contact inhibition of growth. After approximately 20 passages in
Wangyou Feng et al.
Heliyon, 9(9), e19760-e19760 (2023-10-09)
Ovarian cancer is insensitive to immunotherapy and has a high mortality rate. CDK4/6 inhibitors (CDK4/6i) regulate the tumor microenvironment and play an antitumor role. Our previous research demonstrated that lymphocyte aggregation (tertiary lymphoid structures, TLSs) was observed after CDK4/6i treatment.
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