PMID- 36188330
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20221004
IS  - 2470-1343 (Electronic)
IS  - 2470-1343 (Linking)
VI  - 7
IP  - 38
DP  - 2022 Sep 27
TI  - Photodynamic Therapy by Glucose Transporter 1-Selective Light Inactivation.
PG  - 34685-34692
LID - 10.1021/acsomega.2c05042 [doi]
AB  - Chromophore-assisted light inactivation (CALI) was applied to molecule-targeted 
      photodynamic therapy (PDT). In order to identify organic photosensitizers 
      suitable for CALI, the carbonic anhydrase II (CAII) ligand, 4-sulfamoylbenzoic 
      acid 1, was conjugated with several photosensitizers to produce compounds 2-7, 
      whose CALI ability was evaluated by measuring their effect on CAII enzymatic 
      activity. Di-iodinated BODIPY (I(2)BODIPY) exhibited excellent CAII inactivation 
      ability, similar to that of Ru(bpy)(3). The glucose-I(2)BODIPY conjugate (8) was 
      synthesized as an inactivation of glucose transporter 1 (GLUT1), a protein 
      overexpressed in many cancer cells. Under light irradiation, 8 exhibited 
      concentration-dependent cytotoxicity with half maximal inhibitory concentration 
      (IC(50)) values of 5.49, 11.14, and 8.73 muM, against human cervical carcinoma 
      (HeLa), human lung carcinoma (A549), and human hepatocellular carcinoma (HepG2) 
      cell lines, respectively. The GLUT1 inhibitor phloretin suppressed the 
      cytotoxicity induced by 8 under light irradiation in a concentration-dependent 
      manner. Western blot analysis indicated that GLUT1 was not detected in cell lines 
      treated with 10 muM 8 under light irradiation. Furthermore, 8 reduced the levels 
      of epidermal growth factor receptor tyrosine kinase (EGFR), phospho-ERK (Y204), 
      and GLUT1 without affecting ERK, alpha-tubulin, and PCNA protein levels, whereas 
      talaporfin sodium, a clinically approved photosensitizer for PDT, nonspecifically 
      reduced intracellular protein levels in HeLa cells, indicating that 8 has a 
      GLUT1-specific inactivation ability and causes light-induced cytotoxicity by 
      modulating the EGFR/MAPK signaling pathway.
CI  - (c) 2022 The Authors. Published by American Chemical Society.
FAU - Miura, Kazuki
AU  - Miura K
AUID- ORCID: 0000-0003-4514-6305
AD  - Laboratory for Chemistry and Life Science, Institute of Innovative Research, 
      Tokyo Institute of Technology, 4259 Nagatsuta-cho, Midori-ku, Yokohama 226-8503, 
      Japan.
FAU - Wen, Yijin
AU  - Wen Y
AD  - School of Life Science and Technology, Tokyo Institute of Technology, 4259 
      Nagatsuta-cho, Midori-ku, Yokohama 226-8501, Japan.
FAU - Tsushima, Michihiko
AU  - Tsushima M
AD  - School of Life Science and Technology, Tokyo Institute of Technology, 4259 
      Nagatsuta-cho, Midori-ku, Yokohama 226-8501, Japan.
FAU - Nakamura, Hiroyuki
AU  - Nakamura H
AUID- ORCID: 0000-0002-4511-2984
AD  - Laboratory for Chemistry and Life Science, Institute of Innovative Research, 
      Tokyo Institute of Technology, 4259 Nagatsuta-cho, Midori-ku, Yokohama 226-8503, 
      Japan.
LA  - eng
PT  - Journal Article
DEP - 20220916
PL  - United States
TA  - ACS Omega
JT  - ACS omega
JID - 101691658
PMC - PMC9520747
COIS- The authors declare no competing financial interest.
EDAT- 2022/10/04 06:00
MHDA- 2022/10/04 06:01
PMCR- 2022/09/16
CRDT- 2022/10/03 05:06
PHST- 2022/08/07 00:00 [received]
PHST- 2022/09/07 00:00 [accepted]
PHST- 2022/10/03 05:06 [entrez]
PHST- 2022/10/04 06:00 [pubmed]
PHST- 2022/10/04 06:01 [medline]
PHST- 2022/09/16 00:00 [pmc-release]
AID - 10.1021/acsomega.2c05042 [doi]
PST - epublish
SO  - ACS Omega. 2022 Sep 16;7(38):34685-34692. doi: 10.1021/acsomega.2c05042. 
      eCollection 2022 Sep 27.