Recombinant protein rVP1 upregulates BECN1-independent autophagy, MAPK1/3 phosphorylation and MMP9 activity via WIPI1/WIPI2 to promote macrophage migration

Liao, Chiao Chun; Ho, Ming‐Yi; Liang, Shu‐Mei; Liang, Chi-Ming

doi:10.4161/auto.22379

Cited by 38 publications

(39 citation statements)

References 36 publications

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“…Higher concentrations (30 µM) did induce apoptosis in these cells. Other studies reported that urolithin A induced apoptosis in colon cancer HT‐29 cells (at 25, 50, and 100 µM) and prostate cancer LNCaP cells (at 40 µM) . Our studies suggested that the anticancer effects of urolithin A may result, at least in part, from autophagy induction at both lower and higher concentrations, and apoptosis at higher concentrations.…”

Section: Discussionsupporting

confidence: 63%

Metabolite of ellagitannins, urolithin A induces autophagy and inhibits metastasis in human sw620 colorectal cancer cells

Zhao

Shi

Guo

et al. 2017

Molecular Carcinogenesis

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Autophagy is an evolutionarily conserved pathway in which cytoplasmic contents are degraded and recycled. This study found that submicromolar concentrations of urolithin A, a major polyphenol metabolite, induced autophagy in SW620 colorectal cancer (CRC) cells. Exposure to urolithin A also dose‐dependently decreased cell proliferation, delayed cell migration, and decreased matrix metalloproteinas‐9 (MMP‐9) activity. In addition, inhibition of autophagy by Atg5‐siRNA, caspases by Z‐VAD‐FMK suppressed urolithin A‐stimulated cell death and anti‐metastatic effects. Micromolar urolithin A concentrations induced both autophagy and apoptosis. Urolithin A suppressed cell cycle progression and inhibited DNA synthesis. These results suggest that dietary consumption of urolithin A could induce autophagy and inhibit human CRC cell metastasis. Urolithins may thus contribute to CRC treatment and offer an alternative or adjunct chemotherapeutic agent to combat this disease.

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Section: Discussionsupporting

confidence: 63%

Metabolite of ellagitannins, urolithin A induces autophagy and inhibits metastasis in human sw620 colorectal cancer cells

Zhao

Shi

Guo

et al. 2017

Molecular Carcinogenesis

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“…This discipline encompasses any computational tools and methods used to manage, analyze, and manipulate large sets of biological data, which is an essential tool of basic and clinical research. Moreover, it is reported that HSPB1 [23][24][25], TP53 [20][21][22]26], and UNC119 [27][28][29] are associated with proliferation and apoptosis, SUMO4 [30,31] and SETDB1 [32,33] are involved in regulating transcriptional activity, more details, WIP11 [34,35] acts the role in autophagy. These genes centered on PPA1 in tumors functional enrichment maps in our network analysis, which indicates that PPA1 could make a vital effect on gene functions similar to above.…”

Section: Discussionmentioning

confidence: 99%

Clinical significance and functional validation of PPA1 in various tumors

et al. 2016

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The aim of the study was to detect PPA1 expression in various tumors and to investigate the relationship between PPA1 expression and clinicopathological parameters to further analyze its clinical significance. Immunohistochemical staining detected PPA1 expression in 305 noncancerous tissues and 675 tumor tissues, which included 12 different tumor types. QPCR and western blot examined PPA1 expression in tumor‐derived cell lines including those derived from liver, breast, lung, and ovarian cancers. Cell proliferation and apoptosis assays were used to investigate PPA1‐regulated cell growth in tumor cells. Finally, a bioinformatics analysis was used to verify the role of PPA1 in carcinogenesis. Among the 12 types of tumors, PPA1 expression was significantly higher in lung and ovarian cancers (P < 0.001). In lung cancer, PPA1 expression was associated with tumor size, patients’ age, and smoking status, whereas in ovarian cancer, PPA1 expression was associated with pathological grade (P < 0.05). Moreover, we found that PPA1 expression was up‐regulated in lung and ovarian cancer cell lines compared with nontumor cells. In addition, suppression of PPA1 expression by RNA interference in lung and ovarian cancer cells showed increased cell apoptosis and decreased cell proliferation, which was mediated by TP53 and p21 signaling. Notably, a bioinformatics analysis was used to verify the function of PPA1 in the development and progression of tumors. PPA1 expression is significantly higher in many tumors, especially those of lung and ovarian origin, which suggests that PPA1 plays an important role in carcinogenesis and in the development of some tumors.

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“…Migration, invasion and anchorage-independent growth assays were performed in vitro as described previously [6, 24]. Briefly, transwell inserts (8 μm pore; Costar, 3422) were placed into the wells for cell migration assay.…”

Section: Methodsmentioning

confidence: 99%

PATZ1 induces PP4R2 to form a negative feedback loop on IKK/NF-κB signaling in lung cancer

Liang

2016

Oncotarget

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Activation of IKK enhances NF-κB signaling to facilitate cancer cell migration, invasion and metastasis. Here, we uncover the existence of a negative feedback loop of IKK. The transcription factor PATZ1 induces protein phosphatase-4 (PP4) regulatory subunit 2 (PP4R2) in an IKK-dependent manner. PP4R2 enhances the binding of PP4 to phosphorylated IKK to inactivate IKK/NF-κB signaling during sustained stimulation by cellular stimuli such as growth factors and inflammatory mediators. Matched pair studies reveal that primary lung cancers express more PATZ1 and PP4R2 than lymph node metastases in patients. Ectopic PATZ1 decreases invasion/colonization of lung cancers and prolongs the survival of xenograft mice. These effects of PATZ1 are reversed by downregulating PP4R2. Our results suggest that PATZ1 and PP4R2 provide negative feedback on IKK/NF-κB signaling to prevent cancer cells from over-stimulation from cellular stimuli; a decline in PATZ1 and PP4R2 is functionally associated with cancer migration/invasion and agents enhancing PATZ1 and PP4R2 are worth exploring to prevent invasion/metastasis of lung cancers.

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Recombinant protein rVP1 upregulates BECN1-independent autophagy, MAPK1/3 phosphorylation and MMP9 activity via WIPI1/WIPI2 to promote macrophage migration

Cited by 38 publications

References 36 publications

Metabolite of ellagitannins, urolithin A induces autophagy and inhibits metastasis in human sw620 colorectal cancer cells

Metabolite of ellagitannins, urolithin A induces autophagy and inhibits metastasis in human sw620 colorectal cancer cells

Clinical significance and functional validation of PPA1 in various tumors

PATZ1 induces PP4R2 to form a negative feedback loop on IKK/NF-κB signaling in lung cancer

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