Evaluating hepatocellular carcinoma cell lines for tumour samples using within‐sample relative expression orderings of genes

Ao, Lu; Guo, You; Song, Xuekun; Guan, Qingzhou; Zheng, Wenfang; Zhang, Jiahui; Huang, Haiyan; Zou, Yi; Guo, Zheng; Wang, Xianlong

doi:10.1111/liv.13467

Cited by 22 publications

(22 citation statements)

References 37 publications

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“…Furthermore, we selected four HCC cells with different genetic backgrounds to detect the level of GNPDA1 in HCC cells. HepG2 was derived from the liver tissue of a fifteen-year-old Caucasian American male with hepatoblastoma, and does not synthesize hepatitis B virus surface antigen (HBsAg); 29 Hep-3B was derived from the liver tissue of a 8-year-old black male with hepatocellular carcinoma, and synthesizes HBsAg; 30 Huh-7 was derived from the liver tissue of a Japanese man with highly differentiated hepatocellular carcinoma, and does not synthesize HBsAg; HepG2, Hep-3B and Huh7 are highly representative of HCC and show the same metastatic properties of the high-risk metastatic HCC tissues; 31 SMMC-7721 cell line was established in China. We found that compared with L-02, the GNPDA1 levels in SMMC-7721, HepG2 and Huh7 were higher, while there was no significant difference in the level of GNPDA1 between Hep-3B and L-02, which may be affected by HBsAg.…”

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confidence: 99%

<p>Glucosamine-6-Phosphate Isomerase 1 Promotes Tumor Progression and Indicates Poor Prognosis in Hepatocellular Carcinoma</p>

Cheng

Zheng

et al. 2020

CMAR

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Purpose: Reprogramming of metabolic pathways is a hallmark of the pathological changes that occur in cancer cells. Under physiological conditions, glucosamine-6-phosphate isomerase 1 (GNPDA1) promotes the conversion of the hexosamine system to the glycolytic pathway and may, therefore, affect energy metabolism. Low expression of GNPDA1 has been reported in normal liver tissues, however, analysis of the hepatocellular carcinoma (HCC) database in The Cancer Genome Atlas (TCGA) revealed that GNPDA1 was highly expressed in HCC tissues. The purpose of this study was to explore the role of GNPDA1 in HCC. Patients and Methods: We analyzed the expression of GNPDA1 in HCC tissues as well as the clinical outcomes of HCC patients with high or low expression of GNPDA1. Furthermore, the relationship between the expression of GNPDA1 and advanced tumor stage, TNM stage, grade, gender, or metastasis was assessed using high-throughput RNA sequencing data from TCGA HCC cohort and Kaplan-Meier survival analysis. The expression of GNPDA1 in HCC and normal liver cell lines was subsequently detected by qRT-PCR and Western blot analysis. Additionally, the effects of GNPDA1 knockdown in SMMC-7721 and Huh7 cell lines were examined. Cell proliferation, migration, invasion, and apoptosis following knockdown were investigated by the MTT assay and EdU, cell cycle, apoptosis, transwell, and wound healing analyses. Results: There was a significant association between high GNPDA1 expression and advanced tumor stage, TNM stage or grade, but not with gender. High GNPDA1 expression was associated with poor prognosis in patients with HCC. Furthermore, the MTT assay and EdU, cell cycle, apoptosis, wound healing, and transwell analyses revealed that GNPDA1 promoted the proliferation, migration, and invasion of HCC cells and inhibited apoptosis. Conclusion: The results of this study suggest that GNPDA1 may serve as a novel prognostic biomarker and therapeutic target for HCC.

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confidence: 99%

<p>Glucosamine-6-Phosphate Isomerase 1 Promotes Tumor Progression and Indicates Poor Prognosis in Hepatocellular Carcinoma</p>

Cheng

Zheng

et al. 2020

CMAR

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“…The frequent interactions of naturally abundant albumin with cells in the body as well as its wide exogenous applications in the biomedical and pharmaceutical industries (Dennis et al, 2002;Sleep, Cameron & Evans, 2013) prompted us to study the effects of albumin on cells. We have selected HepG2/C3A carcinoma cells because they originate from hepatocytes (Aden et al, 1979) and have been used as a model for studying hepatocellular carcinoma (Chen et al, 2015;Ao et al, 2017) as well as normal hepatocyte functions (Nibourg et al, 2012;Gaskell et al, 2016). Hepatocytes play an important role in the clearance of albumin bound substances (Meijer & Van der Sluijs, 1989), therefore some of these albumin interacting properties can potentially be used in targeting hepatocellular carcinoma or studying the effects of pathologically modified albumin on cellular function.…”

Section: Discussionmentioning

confidence: 99%

Albumin promotes proliferation of G1 arrested serum starved hepatocellular carcinoma cells

Ibrahim

Stange

Dominik

et al. 2020

PeerJ

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Albumin is the most abundant plasma protein and functions as a transport molecule that continuously interacts with various cell types. Because of these properties, albumin has been exploited by the pharmaceutical industry to improve drug delivery into target cells. The immediate effects of albumin on cells, however, require further understanding. The cell interacting properties and pharmaceutical applications of albumin incentivises continual research into the immediate effects of albumin on cells. The HepG2/C3A hepatocellular carcinoma cell line is used as a model for studying cancer pathology as well as liver biosynthesis and cellular responses to drugs. Here we investigated the direct effect of purified albumin on HepG2/C3A cell proliferation in the absence of serum, growth factors and other serum originating albumin bound molecules. We observed that the reduced cell counts in serum starved HepG2/C3A cultures were increased by the inclusion of albumin. Cell cycle analysis demonstrated that the percentage of cells in G1 phase during serum starvation was reduced from 86.4 ± 2.3% to 78.3 ± 3.2% by the inclusion of albumin whereas the percentage of cells in S phase was increased from 6.5 ± 1.5% to 14.3 ± 3.6%. A significant reduction in the cell cycle inhibitor protein, P21, accompanied the changes in the proportions of cell cycle phases upon treatment with albumin. We have also observed that the levels of dead cells determined by DNA fragmentation and membrane permeabilization caused by serum starvation (TUNEL: 16.6 ± 7.2%, ethidium bromide: 13.8 ± 4.8%) were not significantly altered by the inclusion of albumin (11.6 ± 10.2%, ethidium bromide: 16.9 ± 8.9%). Therefore, the increase in cell number was mainly caused by albumin promoting proliferation rather than protection against cell death. These primary findings demonstrate that albumin has immediate effects on HepG2/C3A hepatocellular carcinoma cells. These effects should be taken into consideration when studying the effects of albumin bound drugs or pathological ligands bound to albumin on HepG2/C3A cells.

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“…The frequent interactions of naturally abundant albumin with cells in the body as well as its wide exogenous applications in the biomedical and pharmaceutical industries (Dennis et al, 2002;Sleep, Cameron & Evans, 2013) prompted us to study the effects of albumin on cells. We have selected HepG2/C3A carcinoma cells because they originate from hepatocytes (Aden et al, 1979) and have been used as a model for studying hepatocellular carcinoma (Chen et al, 2015;Ao et al, 2017) as well as normal hepatocyte functions (Nibourg et al, 2012;Gaskell et al, 2016). Hepatocytes play an important role in the clearance of albumin bound substances (Meijer & van der Sluijs, 1989), therefore some of these albumin interacting properties can potentially be used in targeting hepatocellular carcinoma or studying the effects of pathologically modified albumin on cellular function.…”

Section: Discussionmentioning

confidence: 99%

Peer Review #2 of "Albumin promotes proliferation of G1 arrested serum starved hepatocellular carcinoma cells (v0.1)"

2020

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Albumin is the most abundant plasma protein and functions as a transport molecule that continuously interacts with various cell types. Because of these properties, albumin has been exploited by the pharmaceutical industry to improve drug delivery into target cells. The immediate effects of albumin on cells however require further understanding. The cell interacting properties and pharmaceutical applications of albumin incentivises continual research into the immediate effects of albumin on cells. The HepG2/C3A hepatocellular carcinoma cell line is used as a model for studying cancer pathology as well as liver biosynthesis and cellular responses to drugs. Here we investigated the direct effect of purified albumin on HepG2/C3A cell proliferation in the absence of serum, growth factors and other serum originating albumin bound molecules. We observed that the reduced cell counts in serum starved HepG2/C3A cultures were increased by the inclusion of albumin. Cell cycle analysis demonstrated that the percentage of cells in G1 phase during serum starvation was reduced from 86.4±2.3 % to 78.3±3.2 % by the inclusion of albumin whereas the percentage of cells in S phase was increased from 6.5±1.5 % to 14.3±3.6 %. A significant reduction in the cell cycle inhibitor protein, P21, accompanied the changes in the proportions of cell cycle phases upon treatment with albumin. We have also observed that the levels of dead cells determined by DNA fragmentation and membrane permeabilization caused by serum starvation (TUNEL: 16.6 ± 7.2 %, ethidium bromide: 13.8±4.8 %) were not significantly altered by the inclusion of albumin (11.6 ± 10.2 %, ethidium bromide: 16.9 ± 8.9 %). Therefore, the increase in cell number was mainly caused by albumin promoting proliferation rather than protection against cell death. These primary findings demonstrate that albumin has immediate effects on HepG2/C3A hepatocellular carcinoma cells. These effects should be taken into consideration when studying the effects of albumin bound drugs or pathological ligands bound to albumin on HepG2/C3A cells.

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Evaluating hepatocellular carcinoma cell lines for tumour samples using within‐sample relative expression orderings of genes

Abstract: Caution should be taken for using hepatocellular carcinoma cell lines. Our results should be helpful to select proper hepatocellular carcinoma cell lines for biological experiments.

Cited by 22 publications

References 37 publications

<p>Glucosamine-6-Phosphate Isomerase 1 Promotes Tumor Progression and Indicates Poor Prognosis in Hepatocellular Carcinoma</p>

<p>Glucosamine-6-Phosphate Isomerase 1 Promotes Tumor Progression and Indicates Poor Prognosis in Hepatocellular Carcinoma</p>

Albumin promotes proliferation of G1 arrested serum starved hepatocellular carcinoma cells

Peer Review #2 of "Albumin promotes proliferation of G1 arrested serum starved hepatocellular carcinoma cells (v0.1)"

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