# The Inhibition Effect and Mechanism of Staurosporine Isolated from Streptomyces sp. SNC087 Strain on Nasal Polyp

**Authors:** Grace Choi, Eun-Young Lee, Dawoon Chung, Kichul Cho, Woon-Jong Yu, Sang-Jip Nam, Seong-Kook Park, Il-Whan Choi

PMC · DOI: 10.3390/md22010039 · Marine Drugs · 2024-01-11

## TL;DR

This study investigates how staurosporine, a compound from a marine bacteria, can inhibit nasal polyp growth and explores its mechanisms.

## Contribution

The novel contribution is the investigation of staurosporine's inhibitory effects on nasal polyps and its mechanism via the Smad 2 signaling pathway.

## Key findings

- Staurosporine reduces TGF-β1-induced production of Col-1, fibronectin, and α-SMA in nasal polyp fibroblasts.
- The inhibitory effects are mediated through modulation of the Smad 2 signaling pathway.
- Staurosporine also inhibits VEGF production in nasal polyp tissues ex vivo.

## Abstract

This study aims to explore the potential inhibition effects of staurosporine isolated from a Streptomyces sp. SNC087 strain obtained from seawater on nasal polyps. Staurosporine possesses antimicrobial and antihypertensive activities. This research focuses on investigating the effects of staurosporine on suppressing the growth and development of nasal polyps and elucidating the underlying mechanisms involved. The experimental design includes in vitro and ex vivo evaluations to assess the inhibition activity and therapeutic potential of staurosporine against nasal polyps. Nasal polyp-derived fibroblasts (NPDFs) were stimulated with TGF-β1 in the presence of staurosporine. The levels of α-smooth muscle actin (α-SMA), collagen type-I (Col-1), fibronectin, and phosphorylated (p)-Smad 2 were investigated using Western blotting. VEGF expression levels were analyzed in nasal polyp organ cultures treated with staurosporine. TGF-β1 stimulated the production of Col-1, fibronectin, and α-SMA and was attenuated by staurosporine pretreatment. Furthermore, these inhibitory effects were mediated by modulation of the signaling pathway of Smad 2 in TGF-β1-induced NPDFs. Staurosporine also inhibits the production of VEGF in ex vivo NP tissues. The findings from this study will contribute to a better understanding of staurosporine’s role in nasal polyp management and provide insights into its mechanisms of action.

## Linked entities

- **Genes:** TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040], ACTA1 (actin alpha 1, skeletal muscle) [NCBI Gene 58], COL1 (CONSTANS-like 1) [NCBI Gene 831442], fn1.S (fibronectin 1 S homeolog) [NCBI Gene 397744], VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422]
- **Chemicals:** staurosporine (PubChem CID 5279)
- **Diseases:** nasal polyp (MONDO:0006314)

## Full-text entities

- **Genes:** ACTA1 (actin alpha 1, skeletal muscle) [NCBI Gene 58] {aka ACTA, ASMA, CFTD, CFTD1, CFTDM, CMYO2A}, Tgfb1 (transforming growth factor, beta 1) [NCBI Gene 21803] {aka TGF-beta1, TGFbeta1, Tgfb, Tgfb-1}, Acta2 (actin alpha 2, smooth muscle, aorta) [NCBI Gene 11475] {aka 0610041G09Rik, Actvs, SMAalpha, SMalphaA, a-SMA, alphaSMA}, TGFB1 (transforming growth factor beta 1) [NCBI Gene 7040] {aka CAEND1, CED, DPD1, IBDIMDE, LAP, TGF-beta1}, SMAD4 (SMAD family member 4) [NCBI Gene 4089] {aka DPC4, JIP, MADH4, MYHRS}, Fn1 (fibronectin 1) [NCBI Gene 14268] {aka E330027I09, Fn, Fn-1}, VEGFA (vascular endothelial growth factor A) [NCBI Gene 7422] {aka L-VEGF, MVCD1, VEGF, VPF}, SMN1 (survival of motor neuron 1, telomeric) [NCBI Gene 6606] {aka BCD541, GEMIN1, SMA, SMA1, SMA2, SMA3}, SMAD2 (SMAD family member 2) [NCBI Gene 4087] {aka CHTD8, JV18, JV18-1, LDS6, MADH2, MADR2}, FN1 (fibronectin 1) [NCBI Gene 2335] {aka CIG, ED-B, FINC, FN, FNZ, GFND}, Gapdh (glyceraldehyde-3-phosphate dehydrogenase) [NCBI Gene 14433] {aka Gapd}, Smad2 (SMAD family member 2) [NCBI Gene 17126] {aka 7120426M23Rik, Madh2, Madr2, Smad-2, mMad2}, Casp3 (caspase 3) [NCBI Gene 12367] {aka A830040C14Rik, AC-3, CASP-3, CC3, CPP-32, CPP32}
- **Diseases:** polyps (MESH:D011127), leukemia (MESH:D007938), lymphoma (MESH:D008223), chronic inflammation (MESH:D007249), cervical, colon, oral, and breast cancers (MESH:D001943), Fibrosis (MESH:D005355), edema (MESH:D004487), cancer (MESH:D009369), sinusitis (MESH:D012852), injury to people or property (MESH:C000719191), barrier dysfunction (MESH:C536830), melanoma (MESH:D008545), Cytotoxicity (MESH:D064420), tissue degeneration (MESH:D009410), nasal congestion (MESH:D009668), NP (MESH:D009298), allergic reactions (MESH:D004342), runny nose (MESH:D000086722)
- **Species:** Homo sapiens (human, species) [taxon 9606], Saccharomyces cerevisiae (baker's yeast, species) [taxon 4932], Streptomyces sp. (species) [taxon 1931], Mus musculus (house mouse, species) [taxon 10090], Lentzea albida (species) [taxon 65499], Bacteria Latreille et al. 1825 (Bacteria stick insect, genus) [taxon 629395]
- **Cell lines:** S2 — Drosophila melanogaster (Fruit fly), Spontaneously immortalized cell line (CVCL_Z232), SCN087-1 — Rattus norvegicus (Rat), Transformed cell line (CVCL_D049), SNC087 — Homo sapiens (Human), Transformed cell line (CVCL_F335), NPDFs — Sus scrofa (Pig), Transformed cell line (CVCL_A2GJ), 10 — Mus musculus (Mouse), Hybridoma (CVCL_C4R4)

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC10820969/full.md

## References

50 references — full list in the complete paper: https://tomesphere.com/paper/PMC10820969/full.md

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Source: https://tomesphere.com/paper/PMC10820969