Immunomodulatory Protein from Ganoderma microsporum Induces Pro-Death Autophagy through Akt-mTOR-p70S6K Pathway Inhibition in Multidrug Resistant Lung Cancer Cells

Chiu, Ling‐Yen; Hu, Ming-E; Yang, Tsung‐Ying; Hsin, I.; Tsai, Kan-Jen; Sheu, Gwo‐Tarng

doi:10.1371/journal.pone.0125774

Cited by 53 publications

(42 citation statements)

References 44 publications

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“…The present study identified that thapsigargin inhibits p-Akt and p-mTOR protein expression in prostate cancer cells. Chiu et al (22) demonstrated that thapsigargin induces pro-death autophagy through Akt-mTOR-Ribosomal protein S6 kinase β-1 pathway inhibition in multidrug-resistant lung cancer cells. These data suggest the role of thapsigargin-mediated inhibition of the Akt-mTOR pathway in prostate cancer cells.…”

Section: Discussionmentioning

confidence: 99%

Thapsigargin induces apoptosis of prostate cancer through cofilin‑1 and paxillin

Huang

Wang

2018

Oncol Lett

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Abstract. It is widely considered that endoplasmic reticulum stress may rapidly induce apoptosis. The aim of the present study was to investigate the effect of thapsigargin on the induction of apoptosis in prostate cancer cells, and to explore its possible mechanism. A Cell Counting Kit-8 was selected to determine the effect of thapsigargin (0, 1, 10 and 100 nM) on the proliferation of PC3 cells. Cell proliferation of the prostate cancer cells was effectively inhibited by treatment with thapsigargin, and thapsigargin significantly increased the rate of apoptosis and caspase-3/9 activities in prostate cancer cells. The protein expression of phosphorylated (p)-RAC-α serine threonine-protein kinase, p-mechanistic target of rapamycin, F-actin and paxillin were significantly decreased, and cofilin-1 protein expression was significantly increased by treatment with thapsigargin in prostate cancer cells. Overall, the data of the present study revealed that thapsigargin induced apoptosis in prostate cancer cells through cofilin-1 and paxillin.

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Section: Discussionmentioning

confidence: 99%

Thapsigargin induces apoptosis of prostate cancer through cofilin‑1 and paxillin

Huang

Wang

2018

Oncol Lett

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“…At the same time, a lot of Chinese medicine monomers and compounds have been confirmed to show advantages in prolonging the survival period and reversing lung cancer drug resistance [3-5]. Shufeng Jiedu Capsule (SFJDC) was used in experiment and found that it reverses chemoresistance of H69AR.…”

Section: Introductionmentioning

confidence: 99%

Emodin: One Main Ingredient of Shufeng Jiedu Capsule Reverses Chemoresistance of Lung Cancer Cells Through Inhibition of EMT

Yuan

Liao²,

Xue

et al. 2017

Cell Physiol Biochem

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Background: Chemoresistance has become a an important worldwide problem to cancer treatment. Understanding the mechanism of drug resistance is the key to solve this problem and improve the survival of the patient. Doxorubicin and its analogues are widely used as antitumor drugs but many doxorubicin resistant cases have been identified in recent years. Doxorubicin (Dox) resistance is a very serious phenomenon in lung cancer treatment. As we could show previously, Shufeng Jiedu Capsule (SFJDC) can effectively reverse H69AR cells resistance to Dox, thus, the present study was designed to explore the mechanism underlying the effects of the main ingredient Emodin on chemosensitivity of H69AR cells to Dox. Methods: First, the growth inhibition rate of lung cancer cells and normal bronchial epithelial cells (BECs) was determined by MTT. Then, the resistance-induced epithelial-mesenchymal transition (EMT) of H69AR cells was examined by western blot and the effect of Emodin on Twist, Snail or Slug was assayed by Real-time PCR and Western blot. The activation of NF-kappa B was assayed by Western blot. Proliferation, apoptosis, migration and invasion of H69AR cells induced by Twist, Snail and Slug were also assayed by flow cytometry and transwell chamber. Results: The results showed that after administration of Dox (10µM) with different concentrations of Emodin, the cells exhibited a dose-dependent inhibition action to H69AR cells at 48 hours. H69AR induced the expression of Twist, Snail, and Slug when compared with Dox-sensitive H69 cells. The expression of Twist, Snail, and Slug can be effectively inhibited by combination of Dox and Emodin. The reversal of resistance was associated with the inhibition of NF-kappa B. Twist, Snail and Slug promoted proliferation, migration and invasion and inhibited apoptosis. Conclusion: Our data suggest that Emodin can effectively reverse the resistance of H69AR to Dox, an effect paralleled by inhibition of EMT, cell proliferation, apoptosis, migration and invasion.

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“…Previous studies demonstrated that rFIP-gts inhibited A549 cell proliferation by inducing premature senescence and G1 phase arrest [26]; rFIP-gmi induced A549 cell death by activating autophagy through the Akt-mTOR-p70S6K pathway but did not induce apoptotic cell death [27,28]; rLZ-8 mediated the G1 arrest of A549 proliferation via the ribosomal protein S7-MDM2-p53 pathway [29]; FIP-fve inhibits A549 migration via RacGAP1 and suppresses the proliferation of A549 cells via the p53 activation pathway [8]. All these studies indicate that FIPs from Ganoderma spp.…”

Section: Discussionmentioning

confidence: 99%

Identification and Characterisation of a Novel Protein FIP-sch3 from Stachybotrys chartarum

Zhao

et al. 2016

PLoS ONE

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In this study, a novel FIP named FIP-sch3 has been identified and characterised. FIP-sch3 was identified in the ascomycete Stachybotrys chartarum, making it the second FIP to be identified outside the order of Basidiomycota. Recombinant FIP-sch3 (rFIP-shc3) was produced in Escherichia coli and purified using GST-affinity magnetic beads. The bioactive characteristics of FIP-sch3 were compared to those of well-known FIPs LZ-8 from Ganoderma lucidum and FIP-fve from Flammulina velutipes, which were produced and purified using the same method. The purified rFIP-sch3 exhibited a broad spectrum of anti-tumour activity in several types of tumour cells but had no cytotoxicity in normal human embryonic kidney 293 cells. Assays that were implemented to study these properties indicated that rFIP-sch3 significantly suppressed cell proliferation, induced apoptosis and inhibited cell migration in human lung adenocarcinoma A549 cells. The anti-tumour effects of rFIP-sch3 in A549 cells were comparable to those of rLZ-8, but they were significantly greater than those of rFIP-fve. Molecular assays that were built on real-time PCR further revealed potential mechanisms related to apoptosis and migration and that underlie phenotypic effects. These results indicate that FIP-shc3 has a unique anti-tumour bioactive profile, as do other FIPs, which provide a foundation for further studies on anti-tumour mechanisms. Importantly, this study also had convenient access to FIP-sch3 with potential human therapeutic applications.

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Immunomodulatory Protein from Ganoderma microsporum Induces Pro-Death Autophagy through Akt-mTOR-p70S6K Pathway Inhibition in Multidrug Resistant Lung Cancer Cells

Cited by 53 publications

References 44 publications

Thapsigargin induces apoptosis of prostate cancer through cofilin‑1 and paxillin

Thapsigargin induces apoptosis of prostate cancer through cofilin‑1 and paxillin

Emodin: One Main Ingredient of Shufeng Jiedu Capsule Reverses Chemoresistance of Lung Cancer Cells Through Inhibition of EMT

Identification and Characterisation of a Novel Protein FIP-sch3 from Stachybotrys chartarum

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