Antiproliferative effect and autophagy induction of curcumin derivative ZYX02‐Na on the human lung cancer cells A549

Zhou, Guang‐Zhou; Guo, Shuang; Liu, Deng-Xu; Zhang, Lu; Sun, Gang‐Chun

doi:10.1002/jbt.22592

Cited by 5 publications

(7 citation statements)

References 29 publications

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“…In fact, in our previous studies, several Cur analogs, such as MOMI-1, ZYX01, and ZYX02-Na were shown to activate the autophagic process and lead to death of non-small lung cancer A549 cells. [22][23][24] In the present study, EF-24 exhibited similar cellular effect on MCF-7 cancer cells. As expected, fluorescent and electron microscopy observations detected the autophagic vacuoles and F I G U R E 4 Confocal microscopy analysis of the inhibition of autophagosome-lysosome fusion by EF-24.…”

Section: Discussionsupporting

confidence: 68%

Inhibition of autophagic flux by the curcumin analog EF‐24 and its antiproliferative effect on MCF‐7 cancer cells

Wang

Liu

et al. 2023

J Biochem & Molecular Tox

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5‐Bis[(2‐fluorophenyl)methylene]‐4‐piperidinone (EF‐24) is a curcumin analog, which was identified for its physiochemical stability and diverse pharmacological functions. In the present study, EF‐24 was added to the breast cancer cell line MCF‐7 and its cellular effects were characterized. The results indicated that EF‐24 possessed antiproliferative and antimigratory activities on MCF‐7 cells as determined by MTT assay, wound healing, and transwell assay, respectively. In addition, the autophagosomal vesicles could be detected by acridine orange staining and electron microscope analysis in EF‐24‐treated cells. Conversion of LC3‐I to LC3‐II was also investigated following EF‐24 treatment of the cells. However, the expression analysis of p62 and LC3 revealed that EF‐24 could inhibit autophagic flux in MCF‐7 cells. Confocal microscopy suggested that EF‐24 could inhibit the degradation of autophagic vesicles by blocking the fusion of autophagosomes with lysosomes. EF‐24 could also induce apoptosis of MCF‐7 cells as determined by Hoechst 33342 staining, flow cytometry analysis, and western blot analysis. Moreover, treatment of the cells with the autophagy inhibitor 3‐MA enhanced the PARP1 cleavage of EF‐24‐treated MCF‐7 cells, which indicated the crosstalk between autophagy and apoptosis in breast cancer cells. Additional investigation of EF‐24 should be performed in future studies to assess its antiproliferation and antimigratory effects on MCF‐7 cells. However, the current results provide a solid foundation for the potential in vivo anticancer activity of this compound.

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Section: Discussionsupporting

confidence: 68%

Inhibition of autophagic flux by the curcumin analog EF‐24 and its antiproliferative effect on MCF‐7 cancer cells

Wang

Liu

et al. 2023

J Biochem & Molecular Tox

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“…In fact, our previous study demonstrated that curcumin analogs MOMI-1, ZYX01, and ZYX02-Na resulted in the autophagic cell death process of non-small lung cancer cells A549. [25][26][27] In this study, after EF-24 incubation, red autophagic vacuoles, typical autophagic double or multiple membrane structures, and increasing expression of LC3B-II in MDA-MB-231 cells could be detected, suggesting that EF-24 might trigger autophagy in MDA-MB-21 cells.…”

Section: Ef-24 Exerts An Inhibitory Effect Via the Ros-mediating Pathwaysupporting

confidence: 51%

“…In fact, our previous study demonstrated that curcumin analogs MOMI‐1, ZYX01, and ZYX02‐Na resulted in the autophagic cell death process of non‐small lung cancer cells A549. [ 25–27 ] In this study, after EF‐24 incubation, red autophagic vacuoles, typical autophagic double or multiple membrane structures, and increasing expression of LC3B‐II in MDA‐MB‐231 cells could be detected, suggesting that EF‐24 might trigger autophagy in MDA‐MB‐21 cells. EF‐24 could also bring about increase of LC3B‐II level in the presence of the late autophagy inhibitor CQ, confirming that EF‐24 indeed induced complete autophagy rather than blocked the degradation of autophagic vesicles.…”

Section: Discussionmentioning

confidence: 52%

Activation of autophagy promotes the inhibitory effect of curcumin analog EF‐24 against MDA‐MB‐231 cancer cells

Zhao,

Li,

Wang

et al. 2024

J Biochem & Molecular Tox

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Breast cancer is the leading cause of cancer deaths in women worldwide. EF‐24, an analog of curcumin, has been shown to possess promising anticancer effects. However, the underlying mechanism remains elusive. In the present study, the inhibitory effect of EF‐24 against one breast cancer cell line, MDA‐MB‐231, and its anti‐migration ability were assessed by MTT, wound healing, and Transwell assay. Furthermore, we found that EF‐24 could induce initiation of autophagy as evidenced by fluorescence and electron microscope observation. EF‐24 also induced mitochondrial apoptosis in MDA‐MB‐231 cells as detected by Hoechst 33342 staining, flow cytometry analysis, and western blot analysis. In addition, the early autophagy inhibitor 3‐MA could reduce the cleavage of PARP protein and protect cells from EF‐24‐induced apoptosis, while the autophagy inducer (rapamycin) could enhance the anticancer effect of EF‐24 in MDA‐MB‐231 cells, which suggest that EF‐24 induces crosstalk between autophagy and apoptosis, which herein participate in the antiproliferative effect of EF‐24 in breast cancer cells. Moreover, removal of EF‐24‐activated ROS with NAC significantly reversed migration ability of MDA‐MB‐231 cells, indicating that EF‐24 exerted an inhibitory effect through a ROS‐mediating pathway. These results will help to elucidate the antitumor mechanism of curcumin analogs and to explore future potential clinical applications.

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“…Cleavage of Beclin-1 promotes the release of proapoptotic factors from the mitochondria which in turn activate caspases that cleave PARP, thereby triggering apoptosis [50]. Other studies have found anticancer effects of various naturally-derived compounds that were associated with AMPK activation in NSCLC [51][52][53]. Treatment of lung cancer cells (HOP62 and H1975) with the polyphenol ellagic acid resulted in AMPK activation and reduced cell proliferation [51].…”

Section: Discussionmentioning

confidence: 99%

“…Oral administration of ellagic acid reduced the growth of Lewis Lung Carcinoma (LLC) xenografts in mice and was associated with increased levels of phosphorylated AMPK and ACC in tumour tissues [51]. Treatment of A549 NSCLC cells with a synthetic derivative of the polyphenol curcumin inhibited proliferation and migration, and these effects were associated with increased phosphorylation/activation of AMPK [52]. The natural compound phillygenin from the medicinal herb Forsythia suspensa, activated AMPK, inhibited growth, and promoted apoptosis of A549 and SPC-A1 NSCLC cells in vitro and administration of phillygenin to A549 xenografted nude mice resulted in reduced tumour volume [53].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Non-Small Cell Lung Cancer Proliferation and Survival by Rosemary Extract Is Associated with Activation of ERK and AMPK

O’Neill

Moore

Song

et al. 2021

Life

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Non-small cell lung cancer (NSCLC) represents an aggressive form of lung cancer which often develops resistance to chemo- and radiotherapy emphasizing a need to identify novel treatment agents to combat it. Many plants contain compounds with anti-inflammatory, antimicrobial, antidiabetic, and anticancer properties and some plant-derived chemicals are used in the treatment of cancer. A limited number of in vitro and in vivo animal studies provide evidence of anticancer effects of rosemary (Rosmarinus officinalis) extract (RE); however, no studies have explored its role in H1299 NSCLC cells, and its underlying mechanism(s) of action are not understood. The current study examined the effects of RE on H1299 cell proliferation, survival, and migration using specific assays. Additionally, immunoblotting was used to investigate the effects of RE treatment on signalling molecules implicated in cell growth and survival. Treatment with RE dose-dependently inhibited H1299 proliferation with an IC50 value of 19 µg/mL. Similarly, RE dose-dependently reduced cell survival, and this reduction correlated with increased levels of cleaved poly (ADP-ribose) polymerase (PARP), a marker of apoptosis. RE was also able to inhibit cell migration as assessed with a wound healing assay. These cellular effects of RE were associated with an increase in phosphorylated levels of extracellular signal-regulated kinase (ERK), AMP-activated protein kinase (AMPK), and its downstream targets ACC, the mTORC1 protein raptor, and decreased p70S6K phosphorylation. More studies are required to fully examine the effects of RE against NSCLC.

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Antiproliferative effect and autophagy induction of curcumin derivative ZYX02‐Na on the human lung cancer cells A549

Cited by 5 publications

References 29 publications

Inhibition of autophagic flux by the curcumin analog EF‐24 and its antiproliferative effect on MCF‐7 cancer cells

Inhibition of autophagic flux by the curcumin analog EF‐24 and its antiproliferative effect on MCF‐7 cancer cells

Activation of autophagy promotes the inhibitory effect of curcumin analog EF‐24 against MDA‐MB‐231 cancer cells

Inhibition of Non-Small Cell Lung Cancer Proliferation and Survival by Rosemary Extract Is Associated with Activation of ERK and AMPK

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