PMID- 26680865
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20151219
LR  - 20151218
IS  - 1598-2998 (Print)
IS  - 1598-2998 (Linking)
VI  - 34
IP  - 3
DP  - 2002 Jun
TI  - Retinoic Acid Enhances Drug-Induced Cell Death in Anticancer Drug-Resistant Cell 
      Lines.
PG  - 212-7
LID - 10.4143/crt.2002.34.3.212 [doi]
AB  - PURPOSE: Retinoids (RA), a group of vitamin A derivatives, is known to be 
      important for regulation of normal cellular growth and differentiation. RA 
      treatment of various cancers resulted in cell growth inhibition and apoptosis. 
      Therefore, the chemotherapeutic and chemopreventative activities of various types 
      of tumor have been examined. Biological actions of RA are mediated through 
      nuclear receptors, including the retinoic acid receptors (RARs) and retinoid X 
      receptors (RXRs). In this study, we examined the effect of all-trans-retinoic 
      acid (atRA) as an anticancer drug-sensitiser in cancer cell lines and in its 
      drug- resistant cancer cell lines MATERIALS AND METGODS: Cells were maintained by 
      RPMI 1640 medium containing 10% fetal bovine serum. Cells were treated with 1 
      micro M atRA for 48 h, then with the desired concentration of anticancer drug for 
      24 h. Cell viability was measured spectrophotometrically at 540 nm using the MTT 
      [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide] assay. Western 
      blot analyses were performed with the desired antibodies. RESULTS: We 
      investigated if pre-treatment with atRA enhanced the drug-sensitivity of various 
      cancer cell lines to either 5-fluorouracil, adriamycin, or cisplatin. 5-FU 
      (SNU638-F2) and CDDP-resistant cell (SNU638-Cis) lines, from a Korean gastric 
      cancer cell line (SNU638) and the ADR-resistant cells (AD600) was established 
      from a colon cancer cell line (SW620). Treatment of each cell line, with 1 micro 
      M atRA, prior to drug exposure resulted in enhanced cell death in these cell 
      lines. Furthermore, the effect of atRA on growth inhibition, in each 
      drug-resistant cell line, was more obvious than in their parent cell lines. 
      Increased activity of Transglutaminase II (TgaseII) and cleavage of Poly 
      (ADP-ribose) polymerase (PARP) were also observed (western blot analysis. 
      CONCLUSION: Based on our data, we suggest that atRA enhances anticancer 
      drug-induced cell death and reverses the drug-sensitivity of the drug-resistant 
      cancer cell lines.
FAU - Whang, Young Mi
AU  - Whang YM
FAU - Kim, Yeul Hong
AU  - Kim YH
FAU - Shin, Sang Won
AU  - Shin SW
FAU - Kim, Byung Soo
AU  - Kim BS
FAU - Kim, Jun Suk
AU  - Kim JS
FAU - Yoo, Young Do
AU  - Yoo YD
FAU - Park, Sun Hee
AU  - Park SH
LA  - eng
PT  - Journal Article
PL  - Korea (South)
TA  - Cancer Res Treat
JT  - Cancer research and treatment
JID - 101155137
OTO - NOTNLM
OT  - 5-fluorouracil
OT  - Adriamycin
OT  - Cisplatin
OT  - Drug-resistant cancer cell lines
OT  - Retinoic acid
EDAT- 2002/06/01 00:00
MHDA- 2002/06/01 00:01
CRDT- 2015/12/19 06:00
PHST- 2015/12/19 06:00 [entrez]
PHST- 2002/06/01 00:00 [pubmed]
PHST- 2002/06/01 00:01 [medline]
AID - 10.4143/crt.2002.34.3.212 [doi]
PST - ppublish
SO  - Cancer Res Treat. 2002 Jun;34(3):212-7. doi: 10.4143/crt.2002.34.3.212.