5‑Aminolevurinic acid inhibits the proliferation of bladder cancer cells by activating heme synthesis

Nakai, Yasushi; Tatsumi, Yoshihiro; Morizawa, Yosuke; Onishi, Kenta; Miyake, Makito; Oda, Yoshiko; Owari, Takuya; Fujii, Tomomi; Onishi, Sayuri; Tanaka, Nobumichi; Fujimoto, Kiyohide

doi:10.3892/or.2022.8401

Cited by 1 publication

(1 citation statement)

References 27 publications

(39 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cells with high rates of metabolic activity, such as cancer cells, inflammatory cells, and bacteria have lower amounts of ferrochelatase (FECH) , an enzyme capable of metabolizing PpIX, so the production of photoactive porphyrins is more pronounced than in healthy cells [ 25 ]. Reduced FECH expression is present in various tumors such as kidney [ 26 ], bladder [ 27 ], and colorectal [ 28 ]. Low FECH activity of cancer cells causes accumulation of PpIX and other porphyrins in tumors, while normal or high FECH activity results in low accumulation of PpIX in tissues [ 29 ].…”

Section: Introductionmentioning

confidence: 99%

Effect of 5-Aminolevulinic Acid (5-ALA) in “ALADENT” Gel Formulation and Photodynamic Therapy (PDT) against Human Oral and Pancreatic Cancers

D’Antonio,

Marchetti,

Pignatelli

et al. 2024

Biomedicines

View full text Add to dashboard Cite

Oral squamous-cell and pancreatic carcinomas are aggressive cancers with a poor outcome. Photodynamic therapy (PDT) consists of the use of photosensitizer-induced cell and tissue damage that is activated by exposure to visible light. PDT selectively acts on cancer cells, which have an accumulation of photosensitizer superior to that of the normal surrounding tissues. 5-aminolevulinic acid (5-ALA) induces the production of protoporphyrin IX (PpIX), an endogenous photosensitizer activated in PDT. This study aimed to test the effect of a new gel containing 5% v/v 5-ALA (ALAD-PDT) on human oral CAL-27 and pancreatic CAPAN-2 cancer cell lines. The cell lines were incubated in low concentrations of ALAD-PDT (0.05%, 0.10%, 0.20%, 0.40%, 0.75%, 1.0%) for 4 h or 8 h, and then irradiated for 7 min with 630 nm RED light. The cytotoxic effects of ALAD-PDT were measured using the MTS assay. Apoptosis, cell cycle, and ROS assays were performed using flow cytometry. PpIX accumulation was measured using a spectrofluorometer after 10 min and 24 and 48 h of treatment. The viability was extremely reduced at all concentrations, at 4 h for CAPAN-2 and at 8 h for CAL-27. ALAD-PDT induced marked apoptosis rates in both oral and pancreatic cancer cells. Elevated ROS production and appreciable levels of PpIX were detected in both cell lines. The use of ALA-PDT as a topical or intralesional therapy would permit the use of very low doses to achieve effective results and minimize side effects. ALAD-PDT has the potential to play a significant role in complex oral and pancreatic anticancer therapies.

show abstract