Different effects of lysophosphatidic acid receptor-2 (LPA2) and LPA5 on the regulation of chemoresistance in colon cancer cells. 2021

Kaichi Ishimoto, and Akito Minami, and Kanako Minami, and Nanami Ueda, and Toshifumi Tsujiuchi
Division of Molecular Oncology, Department of Life Science, Faculty of Science and Engineering, Kindai University, Higashiosaka, Osaka, Japan.

Lysophosphatidic acid (LPA) is a simple physiological lipid and exhibits several biological functions by binding to G-protein-coupled LPA receptors (LPA receptor-1 (LPA1) to LPA6). The present study aimed to evaluate whether LPA signaling via LPA2 and LPA5 is involved in the chemoresistance to anticancer drugs in colon cancer DLD1 cells. In cell survival assay, cells were treated with fluorouracil (5-FU) every 24 h for 2 days. The cell survival rate to 5-FU of DLD1 cells was significantly decreased by LPA treatment. In the presence of LPA, the cell survival rate to 5-FU was significantly elevated by LPA5 knockdown. Before initiation of the cell survival assay, cells were pretreated with an LPA2 agonist, GRI-977143. The cell survival rate to 5-FU was markedly increased in DLD1 cells treated with GRI-977143. In the presence of GRI-977143, the elevated cell survival rate of DLD1 cells was reduced by LPA2 knockdown. To assess the effects of LPA2 and LPA5 on the enhancement of chemoresistance, long-term 5-FU treated (DLD-5FU) cells were generated from DLD1 cells. The cell survival rate to 5-FU of DLD-5FU cells were significantly elevated by LPA5 knockdown. GRI-977143 treatment increased the cell survival rate to 5-FU of DLD-5FU cells. These results suggest that LPA2 promotes and LPA5 suppresses the acquisition of chemoresistance in colon cancer cells treated with anticancer drugs.

UI MeSH Term Description Entries
D002470 Cell Survival The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability. Cell Viability,Cell Viabilities,Survival, Cell,Viabilities, Cell,Viability, Cell
D003110 Colonic Neoplasms Tumors or cancer of the COLON. Cancer of Colon,Colon Adenocarcinoma,Colon Cancer,Cancer of the Colon,Colon Neoplasms,Colonic Cancer,Neoplasms, Colonic,Adenocarcinoma, Colon,Adenocarcinomas, Colon,Cancer, Colon,Cancer, Colonic,Cancers, Colon,Cancers, Colonic,Colon Adenocarcinomas,Colon Cancers,Colon Neoplasm,Colonic Cancers,Colonic Neoplasm,Neoplasm, Colon,Neoplasm, Colonic,Neoplasms, Colon
D005472 Fluorouracil A pyrimidine analog that is an antineoplastic antimetabolite. It interferes with DNA synthesis by blocking the THYMIDYLATE SYNTHETASE conversion of deoxyuridylic acid to thymidylic acid. 5-FU,5-FU Lederle,5-FU Medac,5-Fluorouracil,5-Fluorouracil-Biosyn,5-HU Hexal,5FU,Adrucil,Carac,Efudex,Efudix,Fluoro-Uracile ICN,Fluoroplex,Fluorouracil Mononitrate,Fluorouracil Monopotassium Salt,Fluorouracil Monosodium Salt,Fluorouracil Potassium Salt,Fluorouracil-GRY,Fluorouracile Dakota,Fluorouracilo Ferrer Far,Fluoruracil,Fluracedyl,Flurodex,Haemato-FU,Neofluor,Onkofluor,Ribofluor,5 FU Lederle,5 FU Medac,5 Fluorouracil,5 Fluorouracil Biosyn,5 HU Hexal,Dakota, Fluorouracile,Fluoro Uracile ICN,Fluorouracil GRY,Haemato FU
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D045744 Cell Line, Tumor A cell line derived from cultured tumor cells. Tumor Cell Line,Cell Lines, Tumor,Line, Tumor Cell,Lines, Tumor Cell,Tumor Cell Lines
D049368 Receptors, Lysophosphatidic Acid A subfamily of lysophospholipid receptors with specificity for LYSOPHOSPHATIDIC ACIDS. LPA Receptor,Lysophosphatidic Acid Receptor,Lysophosphatidic Acid Receptors,EDG7 Protein,Edg-4 Receptor,Edg-7 Receptor,Edg2 Protein,Edg4 Protein,LPA Receptors,LPA-1 Receptor,LPA1 Receptor,LPA2 Receptor,LPA3 Receptor,Receptor, Lysophosphatidic Acid,edg-2 Receptor,vzg-1 Receptor,Acid Receptor, Lysophosphatidic,Acid Receptors, Lysophosphatidic,Edg 4 Receptor,Edg 7 Receptor,LPA 1 Receptor,Receptor, Edg-4,Receptor, Edg-7,Receptor, LPA,Receptor, LPA1,Receptor, LPA2,Receptor, LPA3,Receptor, edg-2,Receptor, vzg-1,Receptors, LPA,edg 2 Receptor,vzg 1 Receptor
D055785 Gene Knockdown Techniques The artificial induction of GENE SILENCING by the use of RNA INTERFERENCE to reduce the expression of a specific gene. It includes the use of DOUBLE-STRANDED RNA, such as SMALL INTERFERING RNA and RNA containing HAIRPIN LOOP SEQUENCE, and ANTI-SENSE OLIGONUCLEOTIDES. Gene Knock Down Techniques,Gene Knock Down,Gene Knock-Down,Gene Knock-Down Techniques,Gene Knockdown,Gene Knock Downs,Gene Knock-Down Technique,Gene Knock-Downs,Gene Knockdown Technique,Gene Knockdowns,Knock Down, Gene,Knock Downs, Gene,Knock-Down Technique, Gene,Knock-Down Techniques, Gene,Knock-Down, Gene,Knock-Downs, Gene,Knockdown Technique, Gene,Knockdown Techniques, Gene,Knockdown, Gene,Knockdowns, Gene,Technique, Gene Knock-Down,Technique, Gene Knockdown,Techniques, Gene Knock-Down,Techniques, Gene Knockdown
D019008 Drug Resistance, Neoplasm Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures. Antibiotic Resistance, Neoplasm,Antineoplastic Drug Resistance,Drug Resistance, Antineoplastic,Antineoplastic Agent Resistance,Neoplasm Drug Resistance,Resistance, Antineoplastic Agent,Resistance, Antineoplastic Drug

Related Publications

Kaichi Ishimoto, and Akito Minami, and Kanako Minami, and Nanami Ueda, and Toshifumi Tsujiuchi
January 2021, Frontiers in cellular neuroscience,
Kaichi Ishimoto, and Akito Minami, and Kanako Minami, and Nanami Ueda, and Toshifumi Tsujiuchi
January 2023, International journal of radiation biology,
Kaichi Ishimoto, and Akito Minami, and Kanako Minami, and Nanami Ueda, and Toshifumi Tsujiuchi
January 2020, Frontiers in molecular neuroscience,
Kaichi Ishimoto, and Akito Minami, and Kanako Minami, and Nanami Ueda, and Toshifumi Tsujiuchi
July 2005, American journal of physiology. Cell physiology,
Kaichi Ishimoto, and Akito Minami, and Kanako Minami, and Nanami Ueda, and Toshifumi Tsujiuchi
July 2021, FEBS letters,
Kaichi Ishimoto, and Akito Minami, and Kanako Minami, and Nanami Ueda, and Toshifumi Tsujiuchi
December 2014, The Journal of biological chemistry,
Kaichi Ishimoto, and Akito Minami, and Kanako Minami, and Nanami Ueda, and Toshifumi Tsujiuchi
September 2009, World journal of gastroenterology,
Kaichi Ishimoto, and Akito Minami, and Kanako Minami, and Nanami Ueda, and Toshifumi Tsujiuchi
August 2008, Cancer science,
Kaichi Ishimoto, and Akito Minami, and Kanako Minami, and Nanami Ueda, and Toshifumi Tsujiuchi
December 2012, Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine,
Kaichi Ishimoto, and Akito Minami, and Kanako Minami, and Nanami Ueda, and Toshifumi Tsujiuchi
January 2016, PloS one,
Copied contents to your clipboard!