HLFHomo sapiens (Human)Cancer cell line

🤖 AI SummaryBased on 15 publications

Quick Overview

HLF is a human hepatocellular carcinoma cell line used in cancer research.

Detailed Summary

HLF is a human hepatocellular carcinoma (HCC) cell line derived from a hepatocellular carcinoma patient. It is widely used in research to study the molecular mechanisms of liver cancer, including genetic alterations, protein expression, and drug sensitivity. HLF has been characterized for its p53 gene status, showing mutations that may contribute to its tumorigenic properties. The cell line is also utilized in studies involving viral infections, such as hepatitis B virus (HBV), and in investigating the role of cytoskeletal-associated proteins like PTPH1. Research on HLF has provided insights into the genetic and molecular changes associated with HCC progression and has been instrumental in identifying potential therapeutic targets.

Research Applications

Cancer researchGenetic and molecular studiesDrug sensitivity profilingViral infection studies (HBV)Protein expression analysis

Key Characteristics

p53 gene mutationsHBV integrationPTPH1 mRNA expressionChromosomal abnormalities
Generated on 6/19/2025

Basic Information

Database IDCVCL_2947
SpeciesHomo sapiens (Human)
Tissue SourceLiver[UBERON:UBERON_0002107]

Donor Information

Age68
Age CategoryAdult
SexMale
Raceasian

Disease Information

DiseaseAdult hepatocellular carcinoma
LineageLiver
SubtypeHepatocellular Carcinoma
OncoTree CodeHCC

DepMap Information

Source TypeHSRRB
Source IDACH-000393_source

Known Sequence Variations

TypeGene/ProteinDescriptionZygosityNoteSource
MutationSimpleTP53p.Gly244Ala (c.731G>C)Unspecified-from parent cell line HLF
MutationSimpleTERTc.1-124C>T (c.228C>T) (C228T)UnspecifiedIn promoterfrom parent cell line Hep-G2

Haplotype Information (STR Profile)

Short Tandem Repeat (STR) profile for cell line authentication.

Amelogenin
X
CSF1PO
10
D13S317
8
D16S539
9,11
D5S818
11
D7S820
11
TH01
6,9
TPOX
8
vWA
16
Gene Expression Profile
Gene expression levels and statistical distribution
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Full DepMap dataset with combined data across cell lines

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Publications

RNA sequencing of hepatobiliary cancer cell lines: data and applications to mutational and transcriptomic profiling.

Umu S.U., Rounge T.B., Roessler S., Lorenzo-Bermejo J.

Cancers (Basel) 12:2510.1-2510.14(2020).

Quantitative proteomics of the Cancer Cell Line Encyclopedia.";

Sellers W.R., Gygi S.P.

Cell 180:387-402.e16(2020).

A pharmacogenomic landscape in human liver cancers.";

Hui L.-J.

Cancer Cell 36:179-193.e11(2019).

Next-generation characterization of the Cancer Cell Line Encyclopedia.

Sellers W.R.

Nature 569:503-508(2019).

Analysis of liver cancer cell lines identifies agents with likely efficacy against hepatocellular carcinoma and markers of response.

Couchy G., Calderaro J., Nault J.-C., Zucman-Rossi J., Rebouissou S.

Gastroenterology 157:760-776(2019).

An interactive resource to probe genetic diversity and estimated ancestry in cancer cell lines.

Dutil J., Chen Z.-H., Monteiro A.N.A., Teer J.K., Eschrich S.A.

Cancer Res. 79:1263-1273(2019).

Characterization of human cancer cell lines by reverse-phase protein arrays.

Liang H.

Cancer Cell 31:225-239(2017).

TCLP: an online cancer cell line catalogue integrating HLA type, predicted neo-epitopes, virus and gene expression.

Loewer M., Sahin U., Castle J.C.

Genome Med. 7:118.1-118.7(2015).

Parallel genome-scale loss of function screens in 216 cancer cell lines for the identification of context-specific genetic dependencies.

Golub T.R., Root D.E., Hahn W.C.

Sci. Data 1:140035-140035(2014).

High frequency of telomerase reverse-transcriptase promoter somatic mutations in hepatocellular carcinoma and preneoplastic lesions.

Laurent C., Laurent A., Cherqui D., Balabaud C., Zucman-Rossi J.

Nat. Commun. 4:2218.1-2218.7(2013).

Genomic landscape of copy number aberrations enables the identification of oncogenic drivers in hepatocellular carcinoma.

Xu J.-C.

Hepatology 58:706-717(2013).

The Cancer Cell Line Encyclopedia enables predictive modelling of anticancer drug sensitivity.

Morrissey M.P., Sellers W.R., Schlegel R., Garraway L.A.

Nature 483:603-607(2012).

Chemosensitivity profile of cancer cell lines and identification of genes determining chemosensitivity by an integrated bioinformatical approach using cDNA arrays.

Yamori T.

Mol. Cancer Ther. 4:399-412(2005).

TFDP1, CUL4A, and CDC16 identified as targets for amplification at 13q34 in hepatocellular carcinomas.

Inazawa J.

Hepatology 35:1476-1484(2002).

Yeast functional assay of the p53 gene status in 11 cell lines and 26 surgical specimens of human hepatocellular carcinoma.

Gao C., Ohashi R., Pu H., Inoue Y., Tsuji T., Miyazaki M., Namba M.

Oncol. Rep. 6:1267-1271(1999).

Screening the p53 status of human cell lines using a yeast functional assay.

Mizusawa H., Tanaka N., Koyama H., Namba M., Kanamaru R., Kuroki T.

Mol. Carcinog. 19:243-253(1997).

p53 gene mutation and integrated hepatitis B viral DNA sequences in human liver cancer cell lines.

Harris C.C.

Carcinogenesis 14:987-992(1993).

Expression of cytoskeletal-associated protein tyrosine phosphatase PTPH1 mRNA in human hepatocellular carcinoma.

Yachi A.

J. Gastroenterol. 29:727-732(1994).

Aberrant elevation of tyrosine-specific phosphorylation in human gastric cancer cells.

Ohnishi Y., Xiao H.-Y., Nagai Y., Takagi H.

Jpn. J. Cancer Res. 82:1428-1435(1991).

Establishment and some biological characteristics of human hepatoma cell lines.

Doi I., Namba M., Sato J.

Gann 66:385-392(1975).

The p53 gene status and other cellular characteristics of human cell lines maintained in our laboratory.

Ohashi R., Namba M.

Tissue Cult. Res. Commun. 16:173-178(1997).

Cellular characteristics and utilization of human hepatoma cell lines which were established in our laboratory and distributed by Japanese Cancer Research Resources Bank.

Namba M., Nakabayashi H., Doi I., Sato J., Miyazaki M.

Tissue Cult. Res. Commun. 12:221-227(1993).

Human hepatoma cell lines.";

Alexander J.J.

(In book chapter) Neoplasms of the liver; Okuda K., Ishak K.G. (eds.); pp.47-56; Springer; Tokyo; Japan (1987).