The putative oncotarget CSN5 controls a transcription-uncorrelated p53-mediated autophagy implicated in cancer cell survival under curcumin treatment

Zhang, Qingyu; Jin, Rui; Zhang, Xian; Sheng, Jipo; Yu, Fang; Tan, Renxiang; Pan, Ying; Junjian, Huang; Kong, Ling-Dong

doi:10.18632/oncotarget.11940

Cited by 10 publications

(7 citation statements)

References 32 publications

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“…Phytochemicals including resveratrol, curcumin, and EGCG inhibit the proliferation of cancer cells by inducing autophagy . We examined whether UA induced autophagy in Ca922 cells.…”

Section: Resultsmentioning

confidence: 99%

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Ursolic acid induces apoptosis and autophagy in oral cancer cells

Lin

Chin

Lee

et al. 2019

Environmental Toxicology

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Oral squamous cell carcinoma (OSCC) is the fifth common cause of cancer mortality in Taiwan with high incidence and recurrence and needs new therapeutic strategies. In this study, ursolic acid (UA), a triterpenoid, was examined the antitumor potency in OSCC cells. Our results showed that UA inhibited the proliferation of OSCC cells in a dose‐ and time‐dependent manner in both Ca922 and SCC2095 oral cancer cells. UA induced caspase‐dependent apoptosis accompanied with the modulation of various biological biomarkers including downregulating Akt/mTOR/NF‐κB signaling, ERK, and p38. In addition, UA inhibited angiogenesis as evidenced by abrogation of migration/invasion and blocking MMP‐2 secretion in Ca922 cells. Interestingly, UA induced autophagy in OSCC cells, as manifested by LC3B‐II conversion and increased p62 expression and accumulation of autophagosomes. Inhibition by autophagy inhibitor enhanced UA‐mediated apoptosis in Ca922 cells. The experiment provides a rationale for using triterpenoid in the treatment of OSCC.

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“…Phytochemicals including resveratrol, curcumin, and EGCG inhibit the proliferation of cancer cells by inducing autophagy . We examined whether UA induced autophagy in Ca922 cells.…”

Section: Resultsmentioning

confidence: 99%

“…Phytochemicals including resveratrol, curcumin, and EGCG inhibit the proliferation of cancer cells by inducing autophagy. [32][33][34] We examined whether UA induced autophagy in Ca922 cells. As shown in Figure 4A, acidic organelles were stained by acridine orange after 24 hours of UA exposure.…”

Section: Ua Induces Autophagy In Osccmentioning

confidence: 99%

Ursolic acid induces apoptosis and autophagy in oral cancer cells

Lin

Chin

Lee

et al. 2019

Environmental Toxicology

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“…Our results indicate that CSN1 does not cooperate with IFT20 in the regulation of TCR trafficking to the IS but do not rule out a role for this protein in signalling events downstream of TCR stimulation. Recent evidence has implicated the COP9 signalosome in another critical quality control pathway, namely, autophagy (Pearce et al, 2009;Su et al, 2011;Zhang et al, 2016). Remarkably, the IFT system has been shown to participate in the first steps of autophagosome formation in ciliated cells (Pampliega et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

The T cell IFT20 interactome reveals new players in immune synapse assembly

Galgano

Onnis

Pappalardo

et al. 2017

Journal of Cell Science

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Sustained signalling at the immune synapse (IS) requires the synaptic delivery of recycling endosome-associated T cell antigen receptors (TCRs). IFT20, a component of the intraflagellar transport system, controls TCR recycling to the IS as a complex with IFT57 and IFT88. Here, we used quantitative mass spectrometry to identify additional interaction partners of IFT20 in Jurkat T cells. In addition to IFT57 and IFT88, the analysis revealed new binding partners, including IFT54 (also known as TRAF3IP1), GMAP-210 (also known as TRIP11), Arp2/3 complex subunit-3 (ARPC3), COP9 signalosome subunit-1 (CSN1, also known as GPS1) and ERGIC-53 (also known as LMAN1). A direct interaction between IFT20 and both IFT54 and GMAP-210 was confirmed in pulldown assays. Confocal imaging of antigen-specific conjugates using T cells depleted of these proteins by RNA interference showed that TCR accumulation and phosphotyrosine signalling at the IS were impaired in the absence of IFT54, ARPC3 or ERGIC-53. Similar to in IFT20-deficient T cells, this defect resulted from a reduced ability of endosomal TCRs to polarize to the IS despite a correct translocation of the centrosome towards the antigen-presenting cell contact. Our data underscore the traffic-related role of an IFT20 complex that includes components of the intracellular trafficking machinery in IS assembly.

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“…Similarly, other studies have demonstrated the capability of p53 to induce autophagy; activation of p53 can cause excess autophagy in cancer cells (25–27). However, inhibition of p53 has also been reported to enhance autophagy under environmental stress conditions (28). Therefore, the present study hypothesized that PEDF may induce excess autophagy via p53 to induce HUVEC death, which may prevent the progression of atherosclerotic plaque formation and tumor growth.…”

Section: Discussionmentioning

confidence: 99%

p53 mediates PEDF‑induced autophagy in human umbilical vein endothelial cells through sestrin2 signaling

Chen

2019

Mol Med Report

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Autophagy is a conserved catabolic process by which cytoplasmic components are delivered into lysosomes for degradation. Pigment epithelium-derived factor (PEDF) has been reported to be associated with autophagy and can induce p53 expression; however, the mechanism relating PEDF with autophagy in endothelial cells remains poorly understood. The present study aimed to investigate the association between the PEDF-p53-sestrin pathway and autophagy in human umbilical vein endothelial cells (HUVECs). PEDF-induced autophagy was examined by fluorescence microscopy and western blot analysis. p53 small interfering (si)RNA and sestrin2 siRNA were constructed and transfected into HUVECs prior to PEDF treatment. The protein expression levels of microtubule-associated protein light chain 3 (LC3) I, LC3 II and p62 were evaluated by western blot analysis, and the mRNA expression levels of p53 and sestrin2 were determined using reverse transcription-quantitative polymerase chain reaction analysis. The regulation of mechanistic target of rapamycin (mTOR) was reflected by p70S6 kinase (p70S6K) and eukaryotic translation initiation factor 4E-binding protein 1 (4E-BP1) protein expression levels, as determined by western blot analysis. PEDF could induce HUVEC autophagy by sequentially inducing p53 and sestrin2 expression, as observed by fluorescence microscopy and western blot analysis. Conversely, the induction of sestrin2 by PEDF was eliminated by p53 siRNA. In addition, p53 siRNA and sestrin2 siRNA could attenuate PEDF-induced HUVEC autophagy. Inhibition of mTOR may be the mechanism responsible for PEDF-induced autophagy; as p70S6K and 4E-BP1 phosphorylation levels were significantly upregulated in p53 siRNA-treated and sestrin2 siRNA-treated groups. The findings of the present study indicated that PEDF may trigger autophagy in HUVECs by inducing p53 and sestrin2 expression, and inhibiting mTOR expression; these findings may contribute to the improved understanding of diseases, including cancer and atherosclerosis.

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The putative oncotarget CSN5 controls a transcription-uncorrelated p53-mediated autophagy implicated in cancer cell survival under curcumin treatment

Cited by 10 publications

References 32 publications

Ursolic acid induces apoptosis and autophagy in oral cancer cells

Ursolic acid induces apoptosis and autophagy in oral cancer cells

The T cell IFT20 interactome reveals new players in immune synapse assembly

p53 mediates PEDF‑induced autophagy in human umbilical vein endothelial cells through sestrin2 signaling

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