SW837

Cat.No.: CSC-6317W

Species: Homo sapiens (Human)

Source: Rectum

Morphology: continuous culture, grown as monolayer, morphology epithelial-like

Culture Properties: monolayer

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Cat.No.
CSC-6317W
Description
Species: human, Caucasian male 53 years old;
Tissue: rectum;
Tumor: adenocarcinoma, grade IV
Species
Homo sapiens (Human)
Source
Rectum
Recommended Medium
SuperCult® Leibovitz's L-15 Medium+10% h.i. FBS+ 2mM L-Glutamine; split confluent culture 1:3-1:4 using trypsin/EDTA; seed at 2-4 x 10^4 cells/cm2; incubate at 37°C without CO2 (close the flask caps)
Culture Properties
monolayer
Morphology
continuous culture, grown as monolayer, morphology epithelial-like
Disease
Rectal Adenocarcinoma
Quality Control
Sterility: mycoplasma negative, HOECHST and PCR
Storage and Shipping
Frozen with Culture medium + 50% FBS + 10% DMSO; ship in dry ice; store in liquid nitrogen
Synonyms
SW-837; SW 837
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

SW837 is a human colorectal cancer cell line originally established from a rectal adenocarcinoma tumor sample of a male patient. It is a model for an advanced colorectal malignancy and is often used as an in vitro model for the study of rectal and colorectal cancer biology. In culture, SW837 cells form an adherent monolayer with an epithelial-like appearance and exhibit stable proliferation in standard culture conditions and is typically maintained in Leibovitz's L-15 or DMEM culture medium with fetal bovine serum supplementation. SW837 cells carry molecular alterations that are known to be oncogenic in colorectal cancer, including activating mutations in KRAS and alterations in the TP53 tumor suppressor pathway. The presence of these mutations results in aberrant activation of pathways controlling cell proliferation, survival, and anti-apoptotic mechanisms, providing a platform to model cellular and molecular processes in colorectal cancer. The cell line also exhibits karyotypic changes that are common in advanced colorectal carcinomas.

In terms of cellular function, SW837 cells exhibit malignant characteristics, such as enhanced proliferation, dysregulated signaling pathways, and sensitivity to chemotherapeutic drugs and targeted inhibitors. SW837, which is dependent on MAPK signaling due to the mutant KRAS, is used to model the impact of MAPK modulation, drug resistance and the testing of inhibitors in colorectal cancer, as well as studies on tumor metabolism, invasion and biomarker discovery.

VASN Promotes CRC Cell Migration, Invasion, Proliferation, and Drug Resistance In Vitro

LARC patients commonly receive adjuvant therapy, however, hidden micrometastases still limit the improvement of OS. Kang's team aims to investigate the impact of VASN in rectal cancer with pulmonary metastasis and understand the underlying molecular mechanisms to guide adjuvant chemotherapy selection.

The expression levels of VASN in different colorectal cancer (CRC) cell lines were examined. The results showed that VASN expression was higher in rectal cancer cell line SW837 than in colon cancer cell lines LOVO and T84 (Fig. 1c). Subsequently, a stable cell line with VASN overexpression or knockdown was constructed and its expression was verified (Fig. 2a, b; Fig. 1e). The Transwell assay revealed that overexpression of VASN enhanced the migration and invasion of CRC cells (Fig. 2c; Fig. 1f), while knockdown of VASN attenuated these effects. Similar effects were also observed in the wound healing experiment (Fig. 2d; Fig. 1g). The IC50 value indicated that VASN overexpression decreased sensitivity to 5-FU, while knockdown increased it (Fig. 2e; Fig. 1h). CCK-8 and colony formation assays showed that VASN overexpression promoted CRC cell proliferation (Fig. 2f, g; Fig. 1i). Western blot and flow cytometry analyses revealed changes in related proteins and cell cycle phases (Fig. 1j). Overall, VASN acts as an oncogene in CRC, promoting cell proliferation and tumorigenesis.

VASN promotes CRC cell migration, invasion, proliferation, and drug resistance in vitro.

Fig. 1. VASN promotes CRC cell migration, invasion, proliferation, and drug resistance in vitro (Kang D, Huang S, et al., 2024).

Vasorin (VASN) overexpression promotes pulmonary metastasis and resistance to adjuvant chemotherapy in patients with locally advanced rectal cancer.

Fig. 2. The oncogene VASN provides a survival advantage to CRC cells (Kang D, Huang S, et al., 2024).

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