TY - JOUR
T1 - Effect of the botanical formula LCS101 on the anti-cancer effects of radiation therapy
AU - Cohen, Zoya
AU - Samuels, Noah
AU - Maimon, Yair
AU - Berger, Raanan
N1 - Publisher Copyright:
© 2018, Springer-Verlag GmbH Germany, part of Springer Nature.
PY - 2019/3/13
Y1 - 2019/3/13
N2 - Background and purpose: The botanical formula LCS101 has been shown in clinical research to reduce chemotherapy-induced toxicities. In pre-clinical research, the formula demonstrated selective anti-cancer effects, in part as a result of radical oxygen species (ROS) activity of the botanical components. The present study examined the interaction between LCS101 and radiation therapy on cancer cell lines. Methods: Incremental doses of LCS101 were added to breast adenocarcinoma (MCF7), prostate (DU145), transitional cell bladder carcinoma (T24), pancreatic epithelioid carcinoma (PANC-1), and osteosarcoma (U20S) cell lines 4 h after single-dose irradiation (range 0.5–4 Gy). Cell viability was tested using sulforhodamine B (SRB) assay after 1 week, with ROS activity examined using 1 mM of the ROS scavenger sodium pyruvate (ROS scavenger), testing cell viability with an SRB assay. Results: The addition of LCS101 to MCF7 (breast) and DU-145 (prostate) cancer cell lines resulted in a dose-dependent increase in the antiproliferative effects of radiation treatment. The addition of pyruvate inhibited radiation-induced cell death in all of the cell lines treated with LCS101. Conclusions: The addition of the botanical formula LCS101 to irradiated cancer cells results in an apparent additive effect, most likely through a ROS-mediated mechanism. These findings support the use of LCS101 by patients undergoing radiation therapy, for both its clinical as well as anti-cancer effects.
AB - Background and purpose: The botanical formula LCS101 has been shown in clinical research to reduce chemotherapy-induced toxicities. In pre-clinical research, the formula demonstrated selective anti-cancer effects, in part as a result of radical oxygen species (ROS) activity of the botanical components. The present study examined the interaction between LCS101 and radiation therapy on cancer cell lines. Methods: Incremental doses of LCS101 were added to breast adenocarcinoma (MCF7), prostate (DU145), transitional cell bladder carcinoma (T24), pancreatic epithelioid carcinoma (PANC-1), and osteosarcoma (U20S) cell lines 4 h after single-dose irradiation (range 0.5–4 Gy). Cell viability was tested using sulforhodamine B (SRB) assay after 1 week, with ROS activity examined using 1 mM of the ROS scavenger sodium pyruvate (ROS scavenger), testing cell viability with an SRB assay. Results: The addition of LCS101 to MCF7 (breast) and DU-145 (prostate) cancer cell lines resulted in a dose-dependent increase in the antiproliferative effects of radiation treatment. The addition of pyruvate inhibited radiation-induced cell death in all of the cell lines treated with LCS101. Conclusions: The addition of the botanical formula LCS101 to irradiated cancer cells results in an apparent additive effect, most likely through a ROS-mediated mechanism. These findings support the use of LCS101 by patients undergoing radiation therapy, for both its clinical as well as anti-cancer effects.
KW - Botanical formula
KW - Cancer
KW - LCS101
KW - Radiation therapy
KW - Radical oxygen species
UR - http://www.scopus.com/inward/record.url?scp=85058012966&partnerID=8YFLogxK
U2 - 10.1007/s00432-018-2812-4
DO - 10.1007/s00432-018-2812-4
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C2 - 30523409
AN - SCOPUS:85058012966
SN - 0171-5216
VL - 145
SP - 609
EP - 613
JO - Journal of Cancer Research and Clinical Oncology
JF - Journal of Cancer Research and Clinical Oncology
IS - 3
ER -