PMID- 35504402
OWN - NLM
STAT- MEDLINE
DCOM- 20220608
LR  - 20220608
IS  - 1638-6183 (Electronic)
IS  - 0300-9084 (Linking)
VI  - 198
DP  - 2022 Jul
TI  - Regulation of apoptosis and autophagy by albendazole in human colon 
      adenocarcinoma cells.
PG  - 155-166
LID - S0300-9084(22)00109-2 [pii]
LID - 10.1016/j.biochi.2022.04.014 [doi]
AB  - Albendazole (ABZ) was initially introduced as an anthelmintic, however, many 
      studies have reported with its anticancer effects. We investigated the anti-tumor 
      effects of ABZ in vitro in human colon adenocarcinoma HCT-15, HCT-116, HT-29, and 
      SW480 cell lines in this study. The cytotoxicity of ABZ was analyzed in colon 
      adenocarcinoma cell lines and normal CCD18Co cells. We found that ABZ induced the 
      subG1 arrest during cell cycle progression, increased the late apoptotic cells, 
      shifted of peak TUNEL-labeled cells peak, and induced apoptosis. Then effects on 
      autophagy activation was confirmed by acridine orange (AO), MDC staining, and 
      immunocytochemistry of LC3. It was observed that ABZ can induce the autophagy 
      activation through modulating the levels of LC3, Atg7, and beclin-1. For 
      mechanistic studies, apoptosis blocker (Z-DEVD-FMK) and autophagy inhibitor 
      (3-MA) were used to confirm that whether ABZ has apoptosis and autophagy specific 
      effects, and reversal in both these cell death processes were noted. The effects 
      of ABZ on AMPK, MAPKs, and ULK induction was also evaluated. We noticed that 
      N-acetyl cysteine (NAC), a broad spectrum antioxidant, can effectively inhibit 
      both apoptosis and autophagy. However, ABZ could even recover suppression of 
      apoptosis and autophagy caused by NAC in colon cancer cells. Therefore, ABZ can 
      potentially up-regulate both the apoptosis and autophagy to significantly 
      suppress tumorigenesis in colorectal cancer cell lines.
CI  - Copyright (c) 2022 Elsevier B.V. and Societe Francaise de Biochimie et Biologie 
      Moleculaire (SFBBM). All rights reserved.
FAU - Jung, Young Yun
AU  - Jung YY
AD  - Department of Science in Korean Medicine, Kyung Hee University, 24 
      Kyungheedae-ro, Dongdaemun-gu, Seoul, 02447, Republic of Korea.
FAU - Baek, Seung Ho
AU  - Baek SH
AD  - College of Korean Medicine, Dongguk University, 32 Dongguk-ro, Ilsandong-gu, 
      Goyang-si, Gyeonggi-do, 10326, Republic of Korea.
FAU - Ha, In Jin
AU  - Ha IJ
AD  - Korean Medicine Clinical Trial Center (K-CTC), Korean Medicine Hospital, Kyung 
      Hee University, Seoul, 02447, Republic of Korea.
FAU - Ahn, Kwang Seok
AU  - Ahn KS
AD  - Department of Science in Korean Medicine, Kyung Hee University, 24 
      Kyungheedae-ro, Dongdaemun-gu, Seoul, 02447, Republic of Korea. Electronic 
      address: ksahn@khu.ac.kr.
LA  - eng
PT  - Journal Article
DEP - 20220430
PL  - France
TA  - Biochimie
JT  - Biochimie
JID - 1264604
RN  - F4216019LN (Albendazole)
SB  - IM
MH  - *Adenocarcinoma/drug therapy/metabolism
MH  - Albendazole/pharmacology
MH  - Apoptosis
MH  - Autophagy
MH  - Cell Line, Tumor
MH  - *Colonic Neoplasms/drug therapy
MH  - Humans
OTO - NOTNLM
OT  - AMPK
OT  - Albendazole
OT  - Apoptosis
OT  - Autophagy
OT  - Human colon adenocarcinoma
OT  - MAPKs
COIS- Declaration of competing interest All authors have no conflicts of interest to 
      declare.
EDAT- 2022/05/04 06:00
MHDA- 2022/06/09 06:00
CRDT- 2022/05/03 19:24
PHST- 2021/09/13 00:00 [received]
PHST- 2022/04/06 00:00 [revised]
PHST- 2022/04/27 00:00 [accepted]
PHST- 2022/05/04 06:00 [pubmed]
PHST- 2022/06/09 06:00 [medline]
PHST- 2022/05/03 19:24 [entrez]
AID - S0300-9084(22)00109-2 [pii]
AID - 10.1016/j.biochi.2022.04.014 [doi]
PST - ppublish
SO  - Biochimie. 2022 Jul;198:155-166. doi: 10.1016/j.biochi.2022.04.014. Epub 2022 Apr 
      30.