title: Characterization of the low pH/low nutrient-resistant LNCaP cell subline             LNCaP-F10.
abstract: Intratumoral regions of low extracellular pH and low nutrition are common             features of solid tumors. Although cancer cells normally die when they are removed             from their environment, a small population of cells survive. In the present study,             the subline LNCaP-F10, of the prostate cancer cell line LNCaP, was isolated and             its low pH/low nutrient-resistant properties were examined. LNCaP-F10 cells were             grown under low-pH/low-nutrient conditions, which caused cell death of the LNCaP             cells. The cell death was associated with oligonucleosomal DNA fragmentation and             poly (ADP-ribose) polymerase (PARP) cleavage, indicating that low-pH/low-nutrient             induced apoptosis in these cells. Significant differences in the expression of             BCL2, BIRC5 and DAPK1 were detected between LNCaP-F10 and LNCaP cells. Tumor growth             caused by implantation of LNCaP-F10 cells into the renal subcapsular space of             nude mice in the absence or presence of prostate stromal cell stimulation was             greater than that caused by implantation of LNCaP cells. LNCaP-F10 cells were             resistant to apoptosis induced by an environment of low-pH/low-nutrient in vitro,             and displayed malignant potential in vivo.
authors.affiliation: Laboratory of Pharmaceutics, Gifu Pharmaceutical University, Gifu, Japan.
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Iguchi
authors.forename: Yuri
authors.initials: Y
authors.lastname: Hayakawa
authors.forename: Kenichiro
authors.initials: K
authors.lastname: Ishii
authors.forename: Kaoru
authors.initials: K
authors.lastname: Matsumoto
authors.forename: Shigeyuki
authors.initials: S
authors.lastname: Usui
authors.forename: Yoshiki
authors.initials: Y
authors.lastname: Sugimura
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Hirano
mesh_terms: D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology; D017209:Apoptosis; D051017:Apoptosis Regulatory Proteins / Q000096:biosynthesis; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000096:biosynthesis; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D053938:DNA Fragmentation; D064550:Death-Associated Protein Kinases; D000077143:Docetaxel; D005047:Etoposide / Q000494:pharmacology; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D006863:Hydrogen-Ion Concentration; D051034:Inhibitor of Apoptosis Proteins / Q000096:biosynthesis; D008297:Male; D051379:Mice; D008819:Mice, Nude; D009368:Neoplasm Transplantation; D017239:Paclitaxel / Q000494:pharmacology; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism*; D011471:Prostatic Neoplasms / Q000378:metabolism / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D000077022:Survivin; D043823:Taxoids / Q000494:pharmacology; D014183:Transplantation, Heterologous
chemical_list: D000970:Antineoplastic Agents; D051017:Apoptosis Regulatory Proteins; C107489:BIRC5 protein, human; D051034:Inhibitor of Apoptosis Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D000077022:Survivin; D043823:Taxoids; D000077143:Docetaxel; D005047:Etoposide; D011065:Poly(ADP-ribose) Polymerases; C579096:DAPK1 protein, human; C579106:Dapk1 protein, mouse; D064550:Death-Associated Protein Kinases; D017871:Calcium-Calmodulin-Dependent Protein Kinases; D017239:Paclitaxel