AsPC-1Homo sapiens (Human)Cancer cell line

Also known as: AsPc-1, Aspc-1, ASPC-1, As-PC1, ASPC1, AsPC1, Aspc1, AsPc1, ASPC

🤖 AI SummaryBased on 9 publications

Quick Overview

Human pancreatic cancer cell line with known metabolic and resistance characteristics.

Detailed Summary

AsPC-1 is a human pancreatic cancer cell line derived from a pancreatic ductal adenocarcinoma. It is widely used in research to study metabolic reprogramming, drug resistance mechanisms, and therapeutic target identification. The cell line exhibits distinct metabolic subtypes, including glycolytic and lipogenic profiles, which influence its response to metabolic inhibitors. Additionally, AsPC-1 has been utilized to investigate cisplatin resistance mechanisms, showing multifactorial resistance involving drug transport, DNA repair, and apoptosis modulation. Its genetic and molecular characteristics make it a valuable model for understanding pancreatic cancer biology and developing targeted therapies.

Research Applications

Metabolic reprogramming studiesDrug resistance mechanismsTherapeutic target identificationCisplatin resistanceMetabolic inhibitor sensitivity

Key Characteristics

Glycolytic and lipogenic metabolic subtypesMultifactorial cisplatin resistanceMetabolic inhibitor sensitivity profiles
Generated on 6/15/2025

Basic Information

Database IDCVCL_0152
SpeciesHomo sapiens (Human)
Tissue SourceAscites[UBERON:UBERON_0007795]

Donor Information

Age62
Age CategoryAdult
SexFemale
Racecaucasian

Disease Information

DiseasePancreatic ductal adenocarcinoma
LineagePancreas
SubtypePancreatic Adenocarcinoma
OncoTree CodePAAD

DepMap Information

Source TypeATCC
Source IDACH-000222_source

Known Sequence Variations

TypeGene/ProteinDescriptionZygosityNoteSource
Gene deletionMAP2K4-Homozygous-PubMed=9331070
MutationSimpleCDKN2Ap.Leu78Hisfs*41 (c.233_234delTC) (p.His93Profs*67, c.276_277delTC)Homozygous-from parent cell line AsPC-1
MutationSimpleKRASp.Gly12Asp (c.35G>A)Unspecified-PubMed=29786757
MutationSimpleSMAD4p.Arg100Thr (c.299G>C)Homozygous-from parent cell line AsPC-1
MutationSimpleTP53p.Cys135Alafs*35 (c.403delT)Heterozygous-PubMed=15367885

Haplotype Information (STR Profile)

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

Amelogenin
X
CSF1PO
10,13
D10S1248
13,14
D12S391
19
D13S317
9,12
D16S539
11
D18S51
18
D19S433
14
D1S1656
12,18.3
D21S11
28,30
D22S1045
15
D2S1338
22,23
D2S441
11,14
D3S1358
16
D5S818
12
D6S1043
11,20
D7S820
12,13
D8S1179
13,15
FGA
24
Penta D
9,12
Penta E
5,12
TH01
7,9.3
TPOX
8,10
vWA
17
Gene Expression Profile
Gene expression levels and statistical distribution
Loading cohorts...
Full DepMap dataset with combined data across cell lines

Loading gene expression data...

Publications

Essential gene profiles in breast, pancreatic, and ovarian cancer cells.

Rottapel R., Neel B.G., Moffat J.

Cancer Discov. 2:172-189(2012).

Pan-cancer proteomic map of 949 human cell lines.";

Robinson P.J., Zhong Q., Garnett M.J., Reddel R.R.

Cancer Cell 40:835-849.e8(2022).

Establishment of highly invasive pancreatic cancer cell lines and the expression of IL-32.

Tanaka S., Nishida T., Hatta H., Nakajima T.

Oncol. Lett. 20:2888-2896(2020).

Quantitative proteomics of the Cancer Cell Line Encyclopedia.";

Sellers W.R., Gygi S.P.

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

Next-generation characterization of the Cancer Cell Line Encyclopedia.

Sellers W.R.

Nature 569:503-508(2019).

Prioritization of cancer therapeutic targets using CRISPR-Cas9 screens.

Stronach E.A., Saez-Rodriguez J., Yusa K., Garnett M.J.

Nature 568:511-516(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).

Differential effector engagement by oncogenic KRAS.";

McCormick F.

Cell Rep. 22:1889-1902(2018).

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

Liang H.

Cancer Cell 31:225-239(2017).

Acquired resistance of pancreatic cancer cells to cisplatin is multifactorial with cell context-dependent involvement of resistance genes.

Mezencev R., Matyunina L.V., Wagner G.T., McDonald J.F.

Cancer Gene Ther. 23:446-453(2016).

A landscape of pharmacogenomic interactions in cancer.";

Wessels L.F.A., Saez-Rodriguez J., McDermott U., Garnett M.J.

Cell 166:740-754(2016).

Resolution of novel pancreatic ductal adenocarcinoma subtypes by global phosphotyrosine profiling.

Biankin A.V., Wu J.-M., Daly R.J.

Mol. Cell. Proteomics 15:2671-2685(2016).

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).

The construction and proliferative effects of a lentiviral vector capable of stably overexpressing SPINK1 gene in human pancreatic cancer AsPC-1 cell line.

Zhang J., Wang D.-M., Hu N., Wang Q., Yu S., Wang J.

Tumor Biol. 37:5847-5855(2016).

Metabolite profiling stratifies pancreatic ductal adenocarcinomas into subtypes with distinct sensitivities to metabolic inhibitors.

Manning G., Settleman J., Hatzivassiliou G., Evangelista M.

Proc. Natl. Acad. Sci. U.S.A. 112:E4410-E4417(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).

A resource for cell line authentication, annotation and quality control.

Neve R.M.

Nature 520:307-311(2015).

A comprehensive transcriptional portrait of human cancer cell lines.

Settleman J., Seshagiri S., Zhang Z.-M.

Nat. Biotechnol. 33:306-312(2015).

KRAS mutational subtype and copy number predict in vitro response of human pancreatic cancer cell lines to MEK inhibition.

Linnartz R., Zubel A., Slamon D.J., Finn R.S.

Br. J. Cancer 111:1788-1801(2014).

The proteomic profile of pancreatic cancer cell lines corresponding to carcinogenesis and metastasis.

Yamada M., Fujii K., Koyama K., Hirohashi S., Kondo T.

J. Proteomics Bioinformatics 2:1-18(2009).

Distribution of characteristic mutations in native ductal adenocarcinoma of the pancreas and pancreatic cancer cell lines.

Saeger H.-D.

Cell Biol. Res. Ther. 2:1000104.1-1000104.5(2013).

Human pancreatic carcinomas and cell lines reveal frequent and multiple alterations in the p53 and Rb-1 tumor-suppressor genes.

Klein-Szanto A.J.P.

Oncogene 7:1503-1511(1992).

Abnormalities of the p53 tumour suppressor gene in human pancreatic cancer.

Lane D.P., Lemoine N.R.

Br. J. Cancer 64:1076-1082(1991).

Characterization of the tumorigenic and metastatic properties of a human pancreatic tumor cell line (AsPC-1) implanted orthotopically into nude mice.

Tan M.H., Chu T.M.

Tumor Biol. 6:89-98(1985).

Cell surface antigens of human ovarian and endometrial carcinoma defined by mouse monoclonal antibodies.

Mattes M.J., Cordon-Cardo C., Lewis J.L. Jr., Old L.J., Lloyd K.O.

Proc. Natl. Acad. Sci. U.S.A. 81:568-572(1984).

Human pancreatic adenocarcinoma: in vitro and in vivo morphology of a new tumor line established from ascites.

Sanders W.H., Berjian R., Douglass H.O. Jr., Martin E.W., Chu T.M.

In Vitro 18:24-34(1982).

Mutations and altered expression of p16INK4 in human cancer.";

Harris C.C.

Proc. Natl. Acad. Sci. U.S.A. 91:11045-11049(1994).

Comparative analysis of mutations in the p53 and K-ras genes in pancreatic cancer.

Berrozpe G., Schaeffer J., Peinado M.A., Real F.X., Perucho M.

Int. J. Cancer 58:185-191(1994).

Frequent alterations of the tumor suppressor genes p53 and DCC in human pancreatic carcinoma.

Arnold R.

Gastroenterology 106:1645-1651(1994).

Human ductal adenocarcinomas of the pancreas express extracellular matrix proteins.

Kloppel G.

Br. J. Cancer 69:144-151(1994).

Human mitogen-activated protein kinase kinase 4 as a candidate tumor suppressor.

Skolnick M.H., Tavtigian S.V.

Cancer Res. 57:4177-4182(1997).

Activation of the urokinase plasminogen activator/urokinase plasminogen activator receptor system and redistribution of E-cadherin are associated with hepatocyte growth factor-induced motility of pancreas tumor cells overexpressing Met.

Real F.X.

Am. J. Pathol. 153:201-212(1998).

Specific chromosomal aberrations and amplification of the AIB1 nuclear receptor coactivator gene in pancreatic carcinomas.

Meltzer P.S., Ried T.

Am. J. Pathol. 154:525-536(1999).

Higher frequency of DPC4/Smad4 alterations in pancreatic cancer cell lines than in primary pancreatic adenocarcinomas.

Chaloupka B., Deiss Y., Simon B., Schudy A.

Cancer Lett. 139:43-49(1999).

Characterization of the mutations of the K-ras, p53, p16, and SMAD4 genes in 15 human pancreatic cancer cell lines.

Sun C.-L., Yamato T., Furukawa T., Ohnishi Y., Kijima H., Horii A.

Oncol. Rep. 8:89-92(2001).

Non-random chromosomal rearrangements in pancreatic cancer cell lines identified by spectral karyotyping.

Sheer D., Moore P.S., Scarpa A., Edwards P.A.W., Lemoine N.R.

Int. J. Cancer 91:350-358(2001).

Genetic profile of 22 pancreatic carcinoma cell lines. Analysis of K-ras, p53, p16 and DPC4/Smad4.

Lohr J.-M., Scarpa A.

Virchows Arch. 439:798-802(2001).

A comprehensive characterization of pancreatic ductal carcinoma cell lines: towards the establishment of an in vitro research platform.

Sipos B., Moser S., Kalthoff H., Torok V., Lohr J.-M., Kloppel G.

Virchows Arch. 442:444-452(2003).

Highly expressed genes in pancreatic ductal adenocarcinomas: a comprehensive characterization and comparison of the transcription profiles obtained from three major technologies.

Kern S.E., Goggins M.G., Hruban R.H.

Cancer Res. 63:8614-8622(2003).

Genome-wide array-based comparative genomic hybridization reveals multiple amplification targets and novel homozygous deletions in pancreatic carcinoma cell lines.

Veltman J.A., van Kessel A.G., Hoglund M.

Cancer Res. 64:3052-3059(2004).

Orthotopic transplantation models of pancreatic adenocarcinoma derived from cell lines and primary tumors and displaying varying metastatic activity.

Hirohashi S.

Pancreas 29:193-203(2004).

Microarray analyses reveal strong influence of DNA copy number alterations on the transcriptional patterns in pancreatic cancer: implications for the interpretation of genomic amplifications.

Gorunova L., van Kessel A.G., Schoenmakers E.F.P.M., Hoglund M.

Oncogene 24:1794-1801(2005).

Synergistic effects of interferon-alpha in combination with chemoradiation on human pancreatic adenocarcinoma.

Marten A.

World J. Gastroenterol. 11:1521-1528(2005).

Identifying allelic loss and homozygous deletions in pancreatic cancer without matched normals using high-density single-nucleotide polymorphism arrays.

Kern S.E.

Cancer Res. 66:7920-7928(2006).

Activation of Wnt signalling in stroma from pancreatic cancer identified by gene expression profiling.

Schackert H.K., Kloppel G., Kalthoff H., Saeger H.-D., Grutzmann R.

J. Cell. Mol. Med. 12:2823-2835(2008).

Identification of SMURF1 as a possible target for 7q21.3-22.1 amplification detected in a pancreatic cancer cell line by in-house array-based comparative genomic hybridization.

Shiratori K., Hirohashi S., Inazawa J., Imoto I.

Cancer Sci. 99:986-994(2008).

A resource for analysis of microRNA expression and function in pancreatic ductal adenocarcinoma cells.

Mendell J.T.

Cancer Biol. Ther. 8:2013-2024(2009).

Signatures of mutation and selection in the cancer genome.";

Deloukas P., Yang F.-T., Campbell P.J., Futreal P.A., Stratton M.R.

Nature 463:893-898(2010).

A genome-wide screen for microdeletions reveals disruption of polarity complex genes in diverse human cancers.

Haber D.A.

Cancer Res. 70:2158-2164(2010).

Phenotype and genotype of pancreatic cancer cell lines.";

Scaife C.L., Firpo M.A., Mulvihill S.J.

Pancreas 39:425-435(2010).

Alterations of the p53 tumor-suppressor gene and ki-ras oncogene in human pancreatic cancer-derived cell-lines with different metastatic potential.

Shimazoe T., Nawata H., Kono A.

Oncol. Rep. 1:1223-1227(1994).

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).