A comprehensive karyotypic analysis on a newly established sarcomatoid hepatocellular carcinoma cell line SH-J1 by comparative genomic hybridization and chromosome painting

Kim, Dae Ghon; Park, Soo Yeun; Kim, Hyun; Chun, Yong Hyuck; Moon, Woo Sung; Park, Sun Hwa

doi:10.1016/s0165-4608(01)00543-x

Cited by 24 publications

(24 citation statements)

References 13 publications

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“…Human HCC cell lines, HLe, HLF and Huh-7, were purchased from the Health science research resources Bank (Osaka, Japan) and HepG2 was obtained from the American type Culture Collection (Manassas, VA). In addition, the sarcomatoid HCC cell line, designated as sH-J1, which was established in our laboratory (19) was used. HepG2, HLe, and Huh-7 cell lines were cultured according to the recommendations of the cell banks.…”

Section: Methodsmentioning

confidence: 99%

Expression and role of SIRT1 in hepatocellular carcinoma

Choi

Bae²,

Jamiyandorj³

et al. 2011

Oncol Rep

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Abstract. silent mating type information regulation 2 homolog 1 (sIrt1) is a multifaceted, nicotinamide adenine dinucleotide-dependent protein deacetylase with involvement in a wide variety of cellular processes ranging from cancer to aging. expression of sIrt1 was evaluated in 90 cases of hepatocellular carcinoma (HCC) and five HCC cell lines. The relationship between the mutation status of p53 and expression of sIrt1 was also investigated in 10 fresh HCC tissues. synthetic small interfering rNA was used to silence sIrt1 gene expression by rNA interference (rNAi), and cell growth and cell cycle progression were assessed. expression of sIrt1 was significantly elevated in the HCC tissues when compared to that of non-tumor tissues (p<0.001). Overexpression of sIrt1 and p53 was observed in 56% (50 of 90) and in 30% (27 of 90) of the HCCs, respectively. expression of sIrt1 showed significant correlation with gender (p=0.023), serum AFP levels (p=0.030), viral infection (p=0.005) and p53 expression (p<0.021). Western blot analysis found no correlation between p53 mutation and expression levels of sIrt1. sIrt1 silencing was found to induce cell growth arrest in HCC cells. these results suggest an association of sIrt1 expression with HCC development and that sIrt1 plays a role in cancer cell growth.

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Section: Methodsmentioning

confidence: 99%

Expression and role of SIRT1 in hepatocellular carcinoma

Choi

Bae²,

Jamiyandorj³

et al. 2011

Oncol Rep

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“…HLE and Huh-7 were purchased from the Health Science Research Resources Bank (Osaka, Japan) and HepG2 was purchased from the American Type Culture Collection (Manassas, VA). In addition, the sarcomatoid HCC cell line, which is designated as SH-J1, was established in our laboratory (20). The HepG2, HLE and Huh-7 cell lines were cultured according to the cell bank's instructions.…”

Section: Methodsmentioning

confidence: 99%

Overexpression of discoidin domain receptor 1 increases the migration and invasion of hepatocellular carcinoma cells in association with matrix metalloproteinase

Park

Kim²,

Lee³

et al. 2007

Oncol Rep

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Abstract. The discoidin domain receptor (DDR) is a class of receptor tyrosine kinases that binds to several collagens. DDR1 is widely expressed in fast-growing invasive tumors of the breast, ovary, esophagus, brain and lung. However, there is little information on the expression of DDR1 in hepatocellular carcinoma (HCC) or its function in migration and invasion. Western blot analysis was performed to determine if four HCC cell lines (HLE, Huh-7, HepG2 and SH-J1) express DDR1. The HLE and Huh-7 cell lines were transfected with two isoforms of DDR1, DDR1a and DDR1b. Immunoprecipitation for DDR1 was then performed. Migration and invasion assays were carried out and the number of migrating cells was counted in 6 randomly selected fields per well under an optical microscope. Zymography was used to determine the level of the matrix metalloproteinase (MMP)-2 and -9 expression. DDR1 was expressed in all four cell lines. In the migration assay, the number of migrating cells was significantly higher in the DDR1a-or DDR1b-overexpressing HLE and Huh-7 cells, particularly after collagen type I stimulation (P<0.001). Collagen type I stimulation activated DDR1. In the invasion assay, there was a significantly higher number of invading cells in the DDR1a-or DDR1b-overexpressing HLE cells and DDR1a-overexpressing Huh-7 cells than in the control (P<0.01). The DDR1a-and DDR1b-overexpressing HLE cells showed a remarkable increase in the MMP-9 and -2 expression, particularly the active MMP-2. The DDR1a-and DDR1b-overexpressing Huh-7 cells showed a slight increase in the MMP-9 and -2 expression. The increased invasiveness of the HCC may be associated with the overexpression of either DDR1a or DDR1b mediated by MMP-2 and -9. Although this study provided one possible mechanism for the invasion of HCC cells, more studies are needed to understand the signal through which DDR1a and DDR1b act in invasion.

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“…The sarcomatous SH-J1 cells were established in our laboratory (14). To determine the effects on growth, cells were cultured on coverslips and treated with the indicated concentrations of parthenolide or vehicle (Me 2 SO) in Dulbecco's modified Eagle medium (Invitrogen) supplemented with 10% fetal bovine serum for 48 h. The cells were fixed with 4% paraformaldehyde in 0.1 M sodium phosphate buffer (pH 7.6) and were then stained with the Diff-Quick stain set (Dade Diagnostics of P. R. Inc., Aguada, Puerto Rico).…”

Section: Methodsmentioning

confidence: 99%

Oxidative Stress-mediated Apoptosis

Wen

You

Lee

et al. 2002

Journal of Biological Chemistry

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290

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The sesquiterpene lactone parthenolide, the principal active component in medicinal plants, has been used conventionally to treat migraines, inflammation, and tumors. However, the antitumor effects of parthenolide and the mechanism(s) involved are poorly understood. We found that parthenolide effectively inhibits hepatoma cell growth in a tumor cell-specific manner and triggers apoptosis of hepatoma cells. Parthenolide triggered apoptosis in invasive sarcomatoid hepatocellular carcinoma cells (SH-J1) as well as in other ordinary hepatoma cells at 5-10 M concentrations and arrested the cell growth (at G 2 /M) at sublethal concentrations (1-3 M). During parthenolide-induced apoptosis, depletion of glutathione, generation of reactive oxygen species, reduction of mitochondrial transmembrane potential, activation of caspases (caspases-7, -8, and -9), overexpression of GADD153 (an oxidative stress or anticancer agent inducible gene), and subsequent apoptotic cell death was observed. This induced apoptosis could be effectively inhibited or abrogated by an antioxidant N-acetyl-L-cysteine, whereas L-buthionine-(S, R)-sulfoximine enhanced it. Furthermore, stable overexpression of GADD153 sensitized the cells to apoptosis induced by parthenolide, and this susceptibility could be reversed by transfection with an antisense to GADD153. Parthenolide did not alter the expression of Bcl-2 or Bcl-X L proteins during apoptosis in hepatoma cells. Oxidative stress may contribute to parthenolide-induced apoptosis and to GADD153 overexpression in a glutathione-sensitive manner. The sensitivity of tumor cells to parthenolide appears to result from the low expression level of the multifunctional detoxification enzyme glutathione S-transferase . Finally, parthenolide and its derivatives may be useful chemotherapeutic agents to treat these invasive cancers.Sesquiterpene lactones are isolated from extracts of Mexican-Indian medicinal plants and have been widely used in indigenous medical practices, including treatment of migraines (1, 2), inflammation (3), and tumors (4, 5). Parthenolide, the major sesquiterpene lactone found in medicinal plants such as feverfew (Tanacetum parthenium), is known to inhibit interleukin 1-and tumor necrosis factor ␣-mediated NF-B activation, which is responsible for its anti-inflammatory activity (6, 7). Parthenolide has been reported to inhibit NF-B by targeting the IB kinase complex (7). Parthenolide also exerts an anti-inflammatory activity by inhibiting the expression of inducible cyclooxygenase, proinflammatory cytokines (8), and inducible nitric-oxide synthase (9). In contrast, the cytotoxic and antitumor effects of sesquiterpene lactones have not been well studied because of their low potency. Recently it has been reported that parthenolide inhibits the in vitro growth of tumor cells in a cytostatic fashion, and it has been proposed that if their selectively cytotoxic or cytostatic actions against tumor cells can be established, sesquiterpene lactones may represent a new class of cancer chemotherapeuti...

show abstract

A comprehensive karyotypic analysis on a newly established sarcomatoid hepatocellular carcinoma cell line SH-J1 by comparative genomic hybridization and chromosome painting

Cited by 24 publications

References 13 publications

Expression and role of SIRT1 in hepatocellular carcinoma

Expression and role of SIRT1 in hepatocellular carcinoma

Overexpression of discoidin domain receptor 1 increases the migration and invasion of hepatocellular carcinoma cells in association with matrix metalloproteinase

Oxidative Stress-mediated Apoptosis

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