Gene expression signature of human HepG2 cell line

Costantini, Susan; Bernardo, Giovanni Di; Cammarota, Marcella; Castello, Giuseppe; Colonna, Giovanni

doi:10.1016/j.gene.2012.12.106

Cited by 77 publications

(57 citation statements)

References 58 publications

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“…Dual-specificity protein phosphatases (Dusp) can dephosphorylate both phosphor-threonine and phosphor-tyrosine residues. Dusp4 was significantly down-regulated in our study, which was consistent with the expression in HepG2 cells [38]. Genetic evidence for the Pla2g2a protecting against tumorigenesis has been demonstrated [39], and the greatest decreased expression was detected in 0.2 μM (-8-fold).…”

Section: Discussionsupporting

confidence: 88%

Transcriptome profiling of malignant transformed rat hepatic stem-like cells by aflatoxin B1

Yang¹,

Ji²,

Chen³

et al. 2014

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Exposure to aflatoxins is strongly associated with hepatocellular carcinoma (HCC). Hepatic progenitor cells have been suggested to participate in the development of HCC. To further explore the molecular basis of aflatoxin-induced carcinogenesis, we utilized transcriptome profiles to examine the global gene expression alterations of malignant transformed rat hepatic stem-like cells. WB-F344 cells were treated with continuous exposure to AFB1 (0.03, 0.1 and 0.2μM), and gained certain characteristics of transformed cells identified by soft agar assay. Microarray analyses of the transformed cells found that 785, 625, and 751 differentially expressed genes were detected in each exposure group, respectively. Hierarchical Clustering revealed that the effect of 0.1 and 0.2μM exposure on the cells was conformable. Importantly, Gene Ontology analysis showed that malignant transformation of the hepatic stem-like cells was closely correlated to biological process, related to cell motion, cell adhesion, immune response and signal transduction. Accordingly, biological pathways was focused mainly on focal adhesion, regulation of actin cytoskeleton, ECM-receptor interaction, MAPK, TGF-β and chemokine signaling pathway. A few genes involved in these pathways exhibited a dose response, including Cav2, Itgb3, Ccl2, Cx3cl1, Pdgfrb and Tmsb4x. These findings would contribute to a growing knowledgebase on the mechanism of aflatoxin-induced hepatocarcinogenesis.

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Section: Discussionsupporting

confidence: 88%

Transcriptome profiling of malignant transformed rat hepatic stem-like cells by aflatoxin B1

Yang¹,

Ji²,

Chen³

et al. 2014

neo

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“…This may be a unique feature of HBL tumors not reported previously, but supported by the decreased expression of EGFR by western blot in the HepG2 hepatoblastoma cell line, compared with four other hepatocellular cancer cell lines, HLF, Huh7, Hi7, and PLC/PRF/547. In another study, the transcriptome of the HepG2 cell line and normal hNHEP hepatocytes was compared using cDNA microarrays48. Several up- and downregulated genes were identified along with differential scores.…”

Section: Discussionsupporting

confidence: 57%

Loss of EGFR-ASAP1 signaling in metastatic and unresectable hepatoblastoma

Ranganathan

Ningappa

Ashokkumar

et al. 2016

Sci Rep

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Hepatoblastoma (HBL), the most common childhood liver cancer is cured with surgical resection after chemotherapy or with liver transplantation if local invasion and multifocality preclude resection. However, variable survival rates of 60–80% and debilitating chemotherapy sequelae argue for more informed treatment selection, which is not possible by grading the Wnt-β-catenin over activity present in most HBL tumors. A hypothesis-generating whole transcriptome analysis shows that HBL tumors removed at transplantation are enriched most for cancer signaling pathways which depend predominantly on epidermal growth factor (EGF) signaling, and to a lesser extent, on aberrant Wnt-β-catenin signaling. We therefore evaluated whether EGFR, ASAP1, ERBB2 and ERBB4, which signal downstream after ligation of EGF, and which show aberrant expression in several other invasive cancers, would also predict HBL tumor invasiveness. Immunohistochemistry of HBL tumors (n = 60), which are histologically heterogeneous, shows that compared with well-differentiated fetal cells, less differentiated embryonal and undifferentiated small cells (SCU) progressively lose EGFR and ASAP1 expression. This trend is exaggerated in unresectable, locally invasive or metastatic tumors, in which embryonal tumor cells are EGFR-negative, while SCU cells are EGFR-negative and ASAP1-negative. Loss of EGFR-ASAP1 signaling characterizes undifferentiated and invasive HBL. EGFR-expressing HBL tumors present novel therapeutic targeting opportunities.

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“…By contrast, the hepatocellular carcinoma HepG2 cell line represents a pure human liver carcinoma cell line free of viral infections, comprises an NRAS mutation, and is often used as an hepatocellular carcinoma model (Hsu et al, 1993;Charette et al, 2010;Costantini et al, 2013). Therefore, the A549 and HepG2 cells were used to produce xenograft tumors in mouse models to evaluate the effectiveness of recombinant pre-miR-34a in the control of tumor growth in vivo.…”

Section: Discussionmentioning

confidence: 99%

Bioengineering Novel Chimeric microRNA-34a for Prodrug Cancer Therapy: High-Yield Expression and Purification, and Structural and Functional Characterization

Wang

Chen

et al. 2015

J Pharmacol Exp Ther

140

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Development of anticancer treatments based on microRNA (miRNA/miR) such as miR-34a replacement therapy is limited to the use of synthetic RNAs with artificial modifications. Herein, we present a new approach to a high-yield and large-scale biosynthesis, in Escherichia coli using transfer RNA (tRNA) scaffold, of chimeric miR-34a agent, which may act as a prodrug for anticancer therapy. The recombinant tRNA fusion pre-miR34a (tRNA/mir-34a) was quickly purified to a high degree of homogeneity (.98%) using anion-exchange fast protein liquid chromatography, whose primary sequence and post-transcriptional modifications were directly characterized by mass spectrometric analyses. Chimeric tRNA/mir-34a showed a favorable cellular stability while it was degradable by several ribonucleases. Deep sequencing and quantitative real-time polymerase chain reaction studies revealed that tRNA-carried pre-miR-34a was precisely processed to mature miR-34a within human carcinoma cells, and the same tRNA fragments were produced from tRNA/ mir-34a and the control tRNA scaffold (tRNA/MSA). Consequently, tRNA/mir-34a inhibited the proliferation of various types of human carcinoma cells in a dose-dependent manner and to a much greater degree than the control tRNA/MSA, which was mechanistically attributable to the reduction of miR-34a target genes. Furthermore, tRNA/mir-34a significantly suppressed the growth of human non-small-cell lung cancer A549 and hepatocarcinoma HepG2 xenograft tumors in mice, compared with the same dose of tRNA/MSA. In addition, recombinant tRNA/mir-34a had no or minimal effect on blood chemistry and interleukin-6 level in mouse models, suggesting that recombinant RNAs were well tolerated. These findings provoke a conversation on producing biologic miRNAs to perform miRNA actions, and point toward a new direction in developing miRNAbased therapies.

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Gene expression signature of human HepG2 cell line

Cited by 77 publications

References 58 publications

Transcriptome profiling of malignant transformed rat hepatic stem-like cells by aflatoxin B1

Transcriptome profiling of malignant transformed rat hepatic stem-like cells by aflatoxin B1

Loss of EGFR-ASAP1 signaling in metastatic and unresectable hepatoblastoma

Bioengineering Novel Chimeric microRNA-34a for Prodrug Cancer Therapy: High-Yield Expression and Purification, and Structural and Functional Characterization

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