Piceatannol enhances Beclin-1 activity to suppress tumor progression and its combination therapy strategy with everolimus in gastric cancer

Huangfu, Longtao; Wang, Xiaoyang; Tian, Shanshan; Chen, Junbing; Fan, Biao; Yao, Qian; Wang, Gangjian; Chen, Cong; Han, Jianda; Xing, Xiaofang; Ji, Jiafu

doi:10.1007/s11427-022-2185-9

Cited by 11 publications

(5 citation statements)

References 36 publications

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“…Notably, piceatannol not only impaired the Beclin-1–Bcl-2 interaction but also enhanced the Beclin-1–UVRAG binding, thus initiating autophagy in gastric cancer cells. Moreover, its combination with an mTOR inhibitor, everolimus, showed a more potent inhibitory effect on SGC7901 and MGC803 cells as well as an anti-tumor effect on the SGC7901 xenograft models, confirming that piceatannol can elicit a synergistic effect with everolimus for gastric cancer therapy 293 .…”

Section: Targeted Beclin-1-regulating Strategies For Cancer Therapymentioning

confidence: 68%

“…Recently, piceatannol ( Fig. 7 E) was confirmed as a promising Beclin-1-targeting agonist, which could directly bind to ECD and reduce Beclin-1 phosphorylation at Ser295 293 . Piceatannol markedly repressed the proliferation of human gastric cancer SGC7901, BGC823, and MKN28 cell lines.…”

Section: Targeted Beclin-1-regulating Strategies For Cancer Therapymentioning

confidence: 99%

“… HER2-positive human breast cancer 46 Tat-SP4 YGRKKRRQRRR-RLISEL(R8)DREKQR(S5)A CCD Enhancing autophagy and the endolysosomal degradation of EGFR A549 (IC 50 = 50.64 μmol/L) H1975 (IC 50 = 43.54 μmol/L) EGFR-overexpressed NSCLS 289 i7-01s-31 YGRKKRRQRRR-VLFN(R8)LVDVIK(S5)RKV CCD Enhancing autophagy and endolysosomal trafficking SKBR3 (IC 50 = 7.12 μmol/L) EGFR- or HER2-driven breast cancer 291 Tat-D3S2 YGRKKRRORRR-GG-SKSGDGNRALQRHVIAR CCD-ECD Inhibiting autophagy Tat-D3S2 inhibited the cell viability of A2780 and SKOV3 during amino acid deprivation by inhibiting autophagy. Ovarian Cancer 287 AG-690/12088124 ECD Inducting autophagy MDA-MB-468 (IC 50 = 9.01 ± 2.31 μmol/L) MDA-MB-231 (IC 50 = 8.25 ± 1.53 μmol/L) MCF-7 (IC 50 = 14.25 ± 1.82 μmol/L) BT-549 (IC 50 = 12.21 ± 1.03 μmol/L) Breast cancer 292 Piceatannol ECD Inducting autophagy C7901 (IC 50 = 2.3 μmol/L) BGC823 (IC 50 = 3.1 μmol/L) MKN28 (IC 50 = 7.3 μmol/L) Gastric cancer 293 TpB Trx tag-AAEQNPIYWARYADWLFTTPLLLLDLALLVDADEGT-CGTNVFNATFHIWHSGQFGT / Inducting autophagy MCF-7 (IC 50 = 12.79 μmol/L, pH = 6.5) SKOV3 (IC 50 = 16.73 μmol/L, pH = 6.5) Breast and ovarian cancer 295 OVV-BECN1 / / Inducting autophagy OVV-BECN1(20 MOI) induces autophagic cell death in K562 and U266 hematologic malignant cells Leukemia and myeloma 299 …”

Section: Targeted Beclin-1-regulating Strategies For Cancer Therapymentioning

confidence: 99%

See 2 more Smart Citations

Targeting autophagy and beyond: Deconvoluting the complexity of Beclin-1 from biological function to cancer therapy

Ye,

Zhang,

Zhu

et al. 2023

Acta Pharmaceutica Sinica B

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Section: Targeted Beclin-1-regulating Strategies For Cancer Therapymentioning

confidence: 68%

Section: Targeted Beclin-1-regulating Strategies For Cancer Therapymentioning

confidence: 99%

Section: Targeted Beclin-1-regulating Strategies For Cancer Therapymentioning

confidence: 99%

See 1 more Smart Citation

Targeting autophagy and beyond: Deconvoluting the complexity of Beclin-1 from biological function to cancer therapy

Ye,

Zhang,

Zhu

et al. 2023

Acta Pharmaceutica Sinica B

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Section: Compounds Targeting Beclin-1mentioning

confidence: 98%

“…Piceatannol is an analog of resveratrol discovered in many plant sources that was revealed to rescue GC via inducing Beclin1 related autophagy in GC cell lines (SGC7901, BGC823, MKN28, MGC803, HGC27, and AGS). Mechanically, piceatannol up‐regulated Beclin1 and impaired the binding of Beclin‐1 to Bcl‐2 (Huangfu et al, 2022). In addition, Liu and his coworkers have reported that metformin induced Beclin‐1 dependent autophagy via targeting AMPK/mTOR signaling pathway in GC cell lines (MKN45, HGC27, SGC7901, BGC823, N87, SNU216, and MGC803) (Liu et al, 2020).…”

Section: Compounds Prevent Gc Via Regulated Cell Deathmentioning

confidence: 99%

Natural products targeting signaling pathways associated with regulated cell death in gastric cancer: Recent advances and perspectives

et al. 2023

Phytotherapy Research

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Gastric cancer (GC) is one of the most serious gastrointestinal malignancies with high morbidity and mortality. The complexity of GC process lies in the multi‐phenotypic linkage regulation, in which regulatory cell death (RCD) is the core link, which largely dominates the fate of GC cells and becomes a key determinant of GC development and prognosis. In recent years, increasing evidence has been reported that natural products can prevent and inhibit the development of GC by regulating RCDs, showing great therapeutic potential. In order to further clarify its key regulatory characteristics, this review focused on specific expressions of RCDs, combined with a variety of signaling pathways and their crosstalk characteristics, sorted out the key targets and action rules of natural products targeting RCD. It is highlighted that a variety of core biological pathways and core targets are involved in the decision of GC cell fate, including the PI3K/Akt signaling pathway, MAPK‐related signaling pathways, p53 signaling pathway, ER stress, Caspase‐8, gasdermin D (GSDMD), and so on. Moreover, natural products target the crosstalk of different RCDs by modulating above signaling pathways. Taken together, these findings suggest that targeting various RCDs in GC with natural products is a promising strategy, providing a reference for further clarifying the molecular mechanism of natural products treating GC, which warrants further investigations in this area.

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Piceatannol induces caspase‐dependent apoptosis by modulating intracellular reactive oxygen species/mitochondrial membrane potential and enhances autophagy in neuroblastoma cells

Güçlü,

Ayan,

Çetinkaya

et al. 2024

J of Applied Toxicology

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The aim of this study was to evaluate the anticancer effects of piceatannol, a natural stilbenoid, on human neuroblastoma cells. In order to accomplish this goal, we performed various cellular assays, including the XTT cell proliferation assay for cell viability, colony formation assay for colony formation capacity, FITC Annexin V and cell death detection kit for apoptosis, matrigel invasion assay for invasion capacity, intracellular reactive oxygen species (ROS) red dye for intracellular ROS levels, TMRM staining method for mitochondrial membrane potential (MMP), and the CYTO‐ID autophagy detection kit for autophagy. Furthermore, we analyzed the expression levels of genes associated with apoptosis and autophagy using RT‐qPCR. Based on our findings, piceatannol exhibited cytotoxic effects on neuroblastoma cells. Besides, treatment with piceatannol at both 50 and 100 μM concentrations for 72 h decreased colony formation, induced apoptosis and autophagy, inhibited cell invasion, decreased MMP, and increased ROS levels in SH‐SY5Y cells. In addition, we observed significant upregulation in the expression levels of CASP8, BECLIN, ATG5, ATG7, and MAPILC3A genes between the two doses. These results suggest that piceatannol enhances autophagic activity and induces caspase‐dependent apoptosis, indicating its potential as a therapeutic agent against neuroblastoma cells.

show abstract

Piceatannol enhances Beclin-1 activity to suppress tumor progression and its combination therapy strategy with everolimus in gastric cancer

Cited by 11 publications

References 36 publications

Targeting autophagy and beyond: Deconvoluting the complexity of Beclin-1 from biological function to cancer therapy

Targeting autophagy and beyond: Deconvoluting the complexity of Beclin-1 from biological function to cancer therapy

Natural products targeting signaling pathways associated with regulated cell death in gastric cancer: Recent advances and perspectives

Piceatannol induces caspase‐dependent apoptosis by modulating intracellular reactive oxygen species/mitochondrial membrane potential and enhances autophagy in neuroblastoma cells

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