The inhibition of PI3K and NFκB promoted curcumin-induced cell cycle arrest at G2/M via altering polyamine metabolism in Bcl-2 overexpressing MCF-7 breast cancer cells

Berrak, Özge; Akkoç, Yunus; Arısan, Elif Damla; Gürkan, Ajda Çoker; Palavan-Ünsal, Narçın

doi:10.1016/j.biopha.2015.12.007

Cited by 60 publications

(41 citation statements)

References 43 publications

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“…However, the different response of PD-0332991 on cell F I G U R E 1 The effect of cell viability of PD-0332991 on Panc-1 and MiaPaCa-2. 17 PD-0332991 inhibited phosphorylation of RB at S780 in Panc-1 cells; however, MiaPaCa-2 cells did not display similar results. After drug treatment, MTT cell viability assay proceeded.…”

Section: Pd-0332991 Induced Cell Cycle Arrestmentioning

confidence: 73%

“…17 Cells were treated with PD-0332991 for 14 days, and colony formation was analyzed with 0.1% of crystal violet staining as described before. Cells were incubated at 37°C and 5% CO 2 incubator (Hera Cell 150i, Thermo Lab Systems, Beverly, MA) and maintained in Dulbecco's modified Eagle medium (DMEM; GIBCO-Life Technologies, Carlsbad, CA) medium supplemented with 1% penicillin/streptomycin (GIBCO, Invitrogen Co, Carlsbad, CA) and 10% fetal bovine serum (FBS; Pan Biotech GmbH, Aidenbach, Germany).…”

Section: Cell Lines and Reagentsmentioning

confidence: 99%

“…17 For, nuclear-cytoplasmic isolation was performed following the NE-PER Nuclear and Cytoplasmic Extraction protocol (Thermo Fisher Scientific). 17 For, nuclear-cytoplasmic isolation was performed following the NE-PER Nuclear and Cytoplasmic Extraction protocol (Thermo Fisher Scientific).…”

Section: Cell Cycle and Western Blot Analysismentioning

confidence: 99%

“…| 509 2.2 | Cell viability, colony formation, and cell survival assay Cell viability response of pancreatic cancer cells to PD-0332991 (0-12.5 µM) was determined for 24 hours using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide cell viability assay as described previously. 17 Cells were treated with PD-0332991 for 14 days, and colony formation was analyzed with 0.1% of crystal violet staining as described before. 17 Cell survival assay was performed to investigate the effect of PD-0332991 (2 and 3 µM) on cell growth.…”

Section: Cell Lines and Reagentsmentioning

confidence: 99%

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Palbociclib, a selective CDK4/6 inhibitor, restricts cell survival and epithelial‐mesenchymal transition in Panc‐1 and MiaPaCa‐2 pancreatic cancer cells

Rencüzoğulları

Yerlikaya

Gürkan

et al. 2019

J of Cellular Biochemistry

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The mortality rate of pancreatic cancer has close parallels to its incidence rate because of limited therapeutics and lack of effective prognosis. Despite various novel chemotherapeutics combinations, the 5‐year survival rate is still under 5%. In the current study, we aimed to modulate the aberrantly activated PI3K/AKT pathway and epithelial‐mesenchymal transition (EMT) signaling with the treatment of CDK4/6 inhibitor PD‐0332991 (palbociclib) in Panc‐1 and MiaPaCa‐2 pancreatic cancer cells. It was found that PD‐0332991 effectively reduced cell viability and proliferation dose‐dependently within 24 hours. In addition, PD‐0332991 induced cell cycle arrest at the G1 phase by downregulation of aberrant expression of CDK4/6 through the dephosphorylation of Rb in each cell lines. Although PD‐0332991 treatment increased epithelial markers and decreased mesenchymal markers, the nuclear translocation of β‐catenin was not prevented by PD‐0332991 treatment, especially in MiaPaCa‐2 cells. Effects of PD‐0332991 on the regulation of PI3K/AKT signaling and its downstream targets such as GSK‐3 were cell type‐dependent. Although the activity of AKT was inhibited in both cell lines, the phosphorylation of GSK‐3β at Ser9 increased only in Panc‐1. In conclusion, PD‐0332991 induced cell cycle arrest and reduced the cell viability of Panc‐1 and MiaPaCa‐2 cells. However, PD‐0332991 differentially affects the regulation of the PI3K/AKT pathway and EMT process in cells due to its distinct influence on Rb and GSK‐3/β‐catenin signaling. Understanding the effect of PD‐0332991 on the aberrantly activated signaling axis may put forward a new therapeutic strategy to reduce the cell viability and metastatic process of pancreatic cancer.

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Section: Pd-0332991 Induced Cell Cycle Arrestmentioning

confidence: 73%

Section: Cell Lines and Reagentsmentioning

confidence: 99%

Section: Cell Cycle and Western Blot Analysismentioning

confidence: 99%

Section: Cell Lines and Reagentsmentioning

confidence: 99%

See 2 more Smart Citations

Palbociclib, a selective CDK4/6 inhibitor, restricts cell survival and epithelial‐mesenchymal transition in Panc‐1 and MiaPaCa‐2 pancreatic cancer cells

Rencüzoğulları

Yerlikaya

Gürkan

et al. 2019

J of Cellular Biochemistry

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“…Polyamines are essential for normal cell growth and differenation, and aberrant polyamine metabolism is known to play an important role in the development of tumors [34, 35]. SSAT is the principal catabolic enzyme responsible for the regulation of intracellular polyamine contents in mammalian cells.…”

Section: Discussionmentioning

confidence: 99%

Spermidine/spermine N1-acetyltransferase regulates cell growth and metastasisviaAKT/β-catenin signaling pathways in hepatocellular and colorectal carcinoma cells

et al. 2016

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Hepatocellular carcinoma (HCC) and colorectal cancer (CRC) are among the most common cancers across the world. Therefore, identifying the potential molecular mechanisms that promote HCC and CRC progression and metastasis are urgently needed. Spermidine/spermine N1-acetyltransferase (SSAT) is a catabolic enzyme that acetylates the high-order polyamines spermine and spermidine, thus decreasing the cellular content of polyamines. Several publications have suggested that depletion of intracellular polyamines inhibited tumor progression and metastasis in various cancer cells. However, whether and how SSAT regulates cell growth, migration and invasion in hepatocellular and colorectal carcinoma cells remains unclear. In this study, depletion of polyamines mediated by SSAT not only attenuated the tumor cell proliferation but also dramatically inhibited cell migration and invasion in hepatocellular and colorectal carcinoma cells. Subsequent investigations revealed introduction of SSAT into HepG2, SMMC7721 hepatocellular carcinoma cells and HCT116 colorectal carcinoma cells significantly suppressed p-AKT, p-GSK3β expression as well as β-catenin nuclear translocation, while inhibition of GSK3β activity or exogenous polyamines could restore SSAT-induced decreases in the protein expression of p-AKT, p-GSK3β and β-catenin. Conversely, knockdown of SSAT in Bel7402 hepatocellular carcinoma cells and HT-29 colorectal carcinoma cells which expressed high levels of SSAT endogenously significantly promoted the expression of p-AKT, p-GSK3β as well as β-catenin nuclear translocation. Taken together, our results indicated depletion of polyamines by SSAT significantly inhibited cell proliferation, migration and invasion through AKT/GSK3β/β-catenin signaling pathway in hepatocellular carcinoma and colorectal cancer cells.

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α‐Pinene inhibits the growth of cervical cancer cells through its proapoptotic activity by regulating the miR‐34a‐5p/Bcl‐2 signaling axis

Huang

Yan

Ding

et al. 2022

Drug Development Research

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Purpose α-pinene was a chemical compound which was extracted from pine needles oil, and it exerted effects on various diseases. However, the effect of α-pinene on cervical cancer had not been reported. The goal of this study was to explore the anti-tumor role of α-pinene.Methods Methyl thiazolyl tetrazolium (MTT) method was used to detect cytotoxicity of α-pinene. Flow cytometry was used to quantify the cell cycle and apoptosis. TUNEL staining was also performed for the revalidation of apoptosis. QRT-PCR and western blot was implemented to detect the expression levels of apoptosis genes and miR-34a-5p. Tumor-bearing nude mouse models was adopted to assess the antitumor action of α-pinene in vivo. ResultsThe results displayed α-pinene restrained proliferation of Hela cells in G1 phase and induced Hela cell apoptosis, which was related to up-regulating expressions of Bax, Bid, Caspase-9, Caspase-3, miR-34a-5p and down-regulating the expression of Bcl-2. Afterwards, α-Pinene could regulate miR-34a-5p/Bcl-2 pathway. Furthermore, α-pinene treatment also induced apoptosis in xenografts tumor models. The uorescence intensity of Bax, Bid, Caspase-9, Caspase-3 increased and uorescence intensity of Bcl-2 decreased.Conclusions Our research demonstrated α-pinene could restrain the development of cervical cancer growth, and it might be an effective chemical compound for therapy of cervical cancer.

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The inhibition of PI3K and NFκB promoted curcumin-induced cell cycle arrest at G2/M via altering polyamine metabolism in Bcl-2 overexpressing MCF-7 breast cancer cells

Cited by 60 publications

References 43 publications

Palbociclib, a selective CDK4/6 inhibitor, restricts cell survival and epithelial‐mesenchymal transition in Panc‐1 and MiaPaCa‐2 pancreatic cancer cells

Palbociclib, a selective CDK4/6 inhibitor, restricts cell survival and epithelial‐mesenchymal transition in Panc‐1 and MiaPaCa‐2 pancreatic cancer cells

Spermidine/spermine N1-acetyltransferase regulates cell growth and metastasisviaAKT/β-catenin signaling pathways in hepatocellular and colorectal carcinoma cells

α‐Pinene inhibits the growth of cervical cancer cells through its proapoptotic activity by regulating the miR‐34a‐5p/Bcl‐2 signaling axis

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