Caffeic acid phenethyl ester induced cell cycle arrest and growth inhibition in androgen-independent prostate cancer cells via regulation of Skp2, p53, p21Cip1 and p27Kip1

Lin, Hui; Lin, Ching Yu; Huo, Chieh; Hsiao, Ping Hsuan; Su, Liang; Jiang, Shih Sheng; Chan, Tzu Min; Chang, Chung Ho; Chen, Li Tzong; Kung, Hsing Jien; Wang, Horng-Dar; Chuu, Chih‐Pin

doi:10.18632/oncotarget.3246

Cited by 66 publications

(52 citation statements)

References 101 publications

(162 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Arsenic trioxide exhibited its antitumor activity via suppression of Skp2 in pancreatic cancer cells (52). Caffeic acid phenethyl ester suppressed cell proliferation and arrested the cell cycle through inactivation of Skp2 in prostate cancer cells (53). Notably, multiple natural agents have been characterized as Skp2 inhibitors (53)(54)(55)(56).…”

Section: Discussionmentioning

confidence: 99%

“…Caffeic acid phenethyl ester suppressed cell proliferation and arrested the cell cycle through inactivation of Skp2 in prostate cancer cells (53). Notably, multiple natural agents have been characterized as Skp2 inhibitors (53)(54)(55)(56). Flavokawain A (FKA) selectively inhibited Skp2 in a proteasome-dependent manner in prostate cancer (57).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Inhibition of Skp2 suppresses the proliferation and invasion of osteosarcoma cells

Ding

Han

et al. 2017

Oncology Reports

View full text Add to dashboard Cite

Abstract. Osteosarcoma (OS) is a common bone tumor that mainly affects children and young adults. S-phase kinase-associated protein 2 (Skp2) has been characterized to play a critical oncogenic role in a variety of human malignancies. However, the biological function of Skp2 in OS remains largely obscure. In the present study, we elucidated the role of Skp2 in cell growth, cell cycle, apoptosis and migration in OS cells. We found that depletion of Skp2 inhibited cell growth in both MG-63 and SW 1353 cells. Moreover, we observed that depletion of Skp2 triggered cell apoptosis in two OS cell lines. Furthermore, downregulation of Skp2 induced cell cycle arrest in the G0/G1 phase in OS cells. Notably, our wound healing assay results revealed that inhibition of Skp2 suppressed cell migration in OS cells. Invariably, our western blot results demonstrated that depletion of Skp2 in OS cells inhibited activation of pAkt and increased p27 expression in OS cells, suggesting that Skp2 exerted its oncogenic function partly through the regulation of Akt and p27. Our findings revealed that targeting Skp2 could be a promising therapeutic strategy for the treatment of OS.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Inhibition of Skp2 suppresses the proliferation and invasion of osteosarcoma cells

Ding

Han

et al. 2017

Oncology Reports

View full text Add to dashboard Cite

show abstract

“…Therefore, compounds that can trigger the expression of tumor suppressor proteins are likely to inhibit the development and transformation of cells into cancerous ones [114] . In a recent study, caffeic acid phenyl esters has been shown to arrest castration resistant prostate cancer (CRPC) cells in the G0/G1 phase of the cell cycle by upregulating p53, p21 and p27 proteins [115]. Confirming this data, knocking down these tumor suppressors using siRNA attenuated the efficacy of caffeic acid phenyl esters [115].…”

Section: Mechanism Of Actionmentioning

confidence: 92%

“…In a recent study, caffeic acid phenyl esters has been shown to arrest castration resistant prostate cancer (CRPC) cells in the G0/G1 phase of the cell cycle by upregulating p53, p21 and p27 proteins [115]. Confirming this data, knocking down these tumor suppressors using siRNA attenuated the efficacy of caffeic acid phenyl esters [115]. Similarly, an increase in the expression of p53 was observed when cervical cancer cells were exposed to caffeic acid [116].…”

Section: Mechanism Of Actionmentioning

confidence: 99%

An overview on the role of dietary phenolics for the treatment of cancers

Anantharaju

Prathima

Vimalambike

et al. 2016

Nutr J

409

248

View full text Add to dashboard Cite

Plant derived phenolic compounds have been shown to inhibit the initiation and progression of cancers by modulating genes regulating key processes such as: (a) oncogenic transformation of normal cells; (b) growth and development of tumors; and (c) angiogenesis and metastasis. Recent studies focusing on identifying the molecular basis of plant phenolics-induced cancer cell death have demonstrated down-regulation of: (a) oncogenic survival kinases such as PI3K and Akt; (b) cell proliferation regulators that include Erk1/2, D-type Cyclins, and Cyclin Dependent Kinases (CDKs); (c) transcription factors such as NF-kβ, NRF2 and STATs; (d) histone deacetylases HDAC1 and HDAC2; and (e) angiogenic factors VEGF, FGFR1 and MIC-1. Furthermore, while inhibiting oncogenic proteins, the phenolic compounds elevate the expression of tumor suppressor proteins p53, PTEN, p21, and p27. In addition, plant phenolic compounds and the herbal extracts rich in phenolic compounds modulate the levels of reactive oxygen species (ROS) in cells thereby regulate cell proliferation, survival and apoptosis. Furthermore, recent studies have demonstrated that phenolic compounds undergo transformation in gut microbiota thereby acquire additional properties that promote their biological activities. In vitro observations, preclinical and epidemiological studies have shown the involvement of plant phenolic acids in retarding the cancer growth. However, to date, there is no clinical trial as such testing the role of plant phenolic compounds for inhibiting tumor growth in humans. More over, several variations in response to phenolic acid rich diets-mediated treatment among individuals have also been reported, raising concerns about whether phenolic acids could be used for treating cancers. Therefore, we have made an attempt to (a) address the key structural features of phenolic acids required for exhibiting potent anti-cancer activity; (b) review the reported findings about the mechanisms of action of phenolic compounds and their transformation by gut microbiota; and (c) update the toxicological aspects and anti-tumor properties of phenolic compounds and extracts containing phenolic compounds in animals.

show abstract

“…Both miR-150 [200] and miR-24 [201] suppresses the expression of p27 among xenograft mice, playing a contributing role on prostate oncogenesis and progression. Besides, administration of a novel compound CAPE displays beneficial anti-tumor effects in prostate cancer cells, primarily via reactivation and nuclear translocation of p27 [202]. Thus, all these evidences suggest that p27-targeted therapy is of great clinical potential as an anti-neoplastic strategy.…”

Section: Functions Of Ampk Signaling Components In Tumorigenesismentioning

confidence: 99%

Functional characterization of AMP-activated protein kinase signaling in tumorigenesis

Cheng

Zhang

et al. 2016

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

View full text Add to dashboard Cite

AMP-activated protein kinase (AMPK) is a ubiquitously expressed metabolic sensor among various species. Specifically, cellular AMPK is phosphorylated and activated under certain stressful conditions, such as energy deprivation, in turn to activate diversified downstream substrates to modulate the adaptive changes and maintain metabolic homeostasis. Recently, emerging evidences have implicated the potential roles of AMPK signaling in tumor initiation and progression. Nevertheless, a comprehensive description on such topic is still in scarcity, especially in combination of its biochemical features with mouse modeling results to elucidate the physiological role of AMPK signaling in tumorigenesis. Hence, we performed this thorough review by summarizing the tumorigenic role of each component along the AMPK signaling, comprising of both its upstream and downstream effectors. Moreover, their functional interplay with the AMPK heterotrimer and exclusive efficacies in carcinogenesis were chiefly explained among genetically altered mice models. Importantly, the pharmaceutical investigations of AMPK relevant medications have also been highlighted. In summary, in this review, we not only elucidate the potential functions of AMPK signaling pathway in governing tumorigenesis, but also potentiate the future targeted strategy aiming for better treatment of aberrant metabolism-associated diseases, including cancer.

show abstract

Caffeic acid phenethyl ester induced cell cycle arrest and growth inhibition in androgen-independent prostate cancer cells via regulation of Skp2, p53, p21Cip1 and p27Kip1

Cited by 66 publications

References 101 publications

Inhibition of Skp2 suppresses the proliferation and invasion of osteosarcoma cells

Inhibition of Skp2 suppresses the proliferation and invasion of osteosarcoma cells

An overview on the role of dietary phenolics for the treatment of cancers

Functional characterization of AMP-activated protein kinase signaling in tumorigenesis

Contact Info

Product

Resources

About