# Effect of photodynamic therapy mediated by hematoporphyrin derivatives on small cell lung cancer H446 cells and bronchial epithelial BEAS-2B cells

**Authors:** Cunzhi Lin, Yuanyuan Zhang, Jiemei Liao, Shichao Cui, Zhe Gao, Weizhong Han

PMC · DOI: 10.1007/s10103-024-04013-2 · 2024-02-17

## TL;DR

This study shows that photodynamic therapy using hematoporphyrin derivatives can reduce the growth of lung cancer and bronchial cells by inducing apoptosis.

## Contribution

The novel contribution is demonstrating the effectiveness of HPD-PDT in inhibiting cancer and bronchial cell proliferation through specific apoptotic pathways.

## Key findings

- HPD-PDT significantly reduced cell viability in H446 and BEAS-2B cells at 15 μg/mL HPD and 50 mW/cm2 laser.
- HPD-PDT increased apoptosis, as shown by increased apoptotic rates and morphological changes.
- HPD-PDT upregulated Bax and Caspase-9 mRNA while downregulating Bcl-2 mRNA, suggesting apoptotic pathway activation.

## Abstract

To investigate the effects of photodynamic therapy (PDT) mediated by hematoporphyrin derivatives (HPD) on the proliferation of small cell lung cancer H446 cells and bronchial epithelial BEAS-2B cells. H446 cells and BEAS-2B cells were cultured in vitro with different concentrations of HPD(0, 5, 10, 12, 15, 20 μg/mL) for 4 h, and then irradiated with 630 nm laser with different energy densities (0, 25, 50, 75, 100 mW/cm2). Cell viability of H446 cells and BEAS-2B cells were detected by CCK8 assay. The cell apoptosis was observed with Annexin V-FTTC/PI double staining and Hoechst 33258. The RT-PCR examination was applied to detect the transcriptional changes of the mRNA of Bax、Bcl-2, and Caspase-9. The results of CCK8 showed that when the HPD was 15 μg/mL and the laser power density reached 50 mW/cm2, the cell viability was significantly decreased compared with the black control group. Hoechst 33258 staining showed that with the increase of HPD concentration, the cell density was reduced, and apoptotic cells increased. Flow cytometry assay revealed that the apoptotic rates of the HPD-PDT group of H446 cells and BEAS-2B cells were significantly different from those of the blank control group. The RT-PCR examination showed that the expression levels of Bax and Caspase-9 mRNA in the HPD-PDT group were up-regulated, while the expression levels of Bcl-2 mRNA were down-regulated significantly. HPD-PDT can inhibit H446 cells and BEAS-2B cells growth. The mechanism may be related to up-regulating the expression levels of Bax and Caspase-9 mRNA and down-regulating the expression levels of Bcl-2 mRNA.

## Linked entities

- **Genes:** BAX (BCL2 associated X, apoptosis regulator) [NCBI Gene 581], BCL2 (BCL2 apoptosis regulator) [NCBI Gene 596], Casp9 (caspase 9) [NCBI Gene 12371]
- **Chemicals:** doxorubicin (PubChem CID 31703)
- **Diseases:** lung cancer (MONDO:0005138)

## Full-text entities

- **Genes:** BCL2 (BCL2 apoptosis regulator) [NCBI Gene 596] {aka Bcl-2, PPP1R50}, ANXA5 (annexin A5) [NCBI Gene 308] {aka ANX5, CPB-I, ENX2, HEL-S-7, PP4, RPRGL3}, BAX (BCL2 associated X, apoptosis regulator) [NCBI Gene 581] {aka BCL2L4}, CASP9 (caspase 9) [NCBI Gene 842] {aka APAF-3, APAF3, ICE-LAP6, MCH6, PPP1R56}
- **Diseases:** small cell lung cancer (MESH:D055752)
- **Chemicals:** FTTC (-), HPD (MESH:D017324), Hoechst 33258 (MESH:D006690)
- **Cell lines:** BEAS-2B — Homo sapiens (Human), Transformed cell line (CVCL_0168)

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC10874342/full.md

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Source: https://tomesphere.com/paper/PMC10874342