Analgesic-antitumor peptide induces apoptosis and inhibits the proliferation of SW480 human colon cancer cells

Gu, Yu; Liu, Shenlin; Ju, Wen-zheng; Li, Chang-Yin; Cao, Peng

doi:10.3892/ol.2012.1049

Cited by 33 publications

(34 citation statements)

References 40 publications

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“…As the expression of ERb gradually increased with calycosin, the levels of IGF-1R decreased, accompanied with attenuated phosphorylation of Akt (Chen et al, 2014). Akt suppresses cell apoptosis by inhibiting Bax (Gu et al, 2013). Bax, as a member of the Bcl-2 family, interacts with the permeability transition pore to lower the mitochondrial membrane potential and release cytochrome c, inducing mitochondrial pathway of apoptosis (Huang et al, 2014;Park et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Genistein induces activation of the mitochondrial apoptosis pathway by inhibiting phosphorylation of Akt in colorectal cancer cells

Qin¹,

Teng²,

Zhu

et al. 2015

Pharmaceutical Biology

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Context: Genistein inhibits the proliferation and induces apoptosis of colorectal cancer cells; however, the underling molecular mechanisms remain to be determined. Aim: The aim of this study was to investigate whether genistein reduces cell viability by suppressing the phosphorylation of AKT and activating the mitochondrial apoptosis pathway in colorectal cancer cells. Materials and methods: The anti-proliferative effects of genistein (0, 25, 50, and 100 mM) on HCT-116 and LoVo cells were assessed using MTT assay. Genistein-induced apoptosis was measured by Hoechst 33258 staining and flow cytometry. The mRNA level of Bax was detected by real-time PCR. The protein levels of Bax, total Akt, and phosphorylated Akt were assessed by western blot. Results: The IC 50 values of genistein were 690, 135, and 61 mM in HCT-116 cells and 204, 135, and 93 mM in LoVo cells after treatment for 24, 48, and 72 h, respectively. After treatment with different concentrations of genistein (0, 25, 50, and 100 mM) for 48 h, the early apoptotic cells in HCT-116 increased from 1.99% ± 0.55% to 6.78% ± 2.12%, 23.16% ± 3.87%, and 36.99% ± 3.76%, respectively. The same concentrations of genistein increased the early apoptotic cells in LoVo from 2.56% ± 1.42% to 3.21% ± 1.52%, 18.22% ± 3.56%, and 23.56% ± 3.02%, respectively. Moreover, genistein increased the mRNA and protein levels of Bax, while it inhibited the phosphorylation of Akt in HCT-116 cells. Conclusion: Genistein inhibited cell proliferation and induced apoptosis of colorectal cancer cells. Genistein induced the mitochondrial pathway of apoptosis in HCT-116 cells by inhibiting phosphorylation of Akt.

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Section: Discussionmentioning

confidence: 99%

Genistein induces activation of the mitochondrial apoptosis pathway by inhibiting phosphorylation of Akt in colorectal cancer cells

Qin¹,

Teng²,

Zhu

et al. 2015

Pharmaceutical Biology

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“…Currently, the antitumor role of the analgesic-antitumor peptide (AGAP) isolated from the scorpion Buthus martensii has been reported. This protein, consisting of a small ubiquitin-related modifier linked with a hexahistidine tag from E. coli , was used as an antitumor peptide, and the main mechanism of action of this peptidomimetic is through cell cycle arrest 91. The recombinant system AGAP showed considerable inhibition of lymphoma and glioma propagation 91.…”

Section: Therapeutic Potential Of Antimicrobial Peptidomimeticsmentioning

confidence: 99%

“…This protein, consisting of a small ubiquitin-related modifier linked with a hexahistidine tag from E. coli , was used as an antitumor peptide, and the main mechanism of action of this peptidomimetic is through cell cycle arrest 91. The recombinant system AGAP showed considerable inhibition of lymphoma and glioma propagation 91. Interestingly, using SW480 human colon cancer cells, it was proposed that recombinant AGAP induces cell cycle arrest in the G0/G1 phase, attended by the decrease in the S phase without significant change in the G2/M phase 91.…”

Section: Therapeutic Potential Of Antimicrobial Peptidomimeticsmentioning

confidence: 99%

Peptidomimetics as a new generation of antimicrobial agents: current progress

Méndez-Samperio¹

2014

IDR

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Antibiotic resistance is an increasing public health concern around the world. Rapid increase in the emergence of multidrug-resistant bacteria has been the target of extensive research efforts to develop a novel class of antibiotics. Antimicrobial peptides (AMPs) are small cationic amphiphilic peptides, which play an important role in the defense against bacterial infections through disruption of their membranes. They have been regarded as a potential source of future antibiotics, owing to a remarkable set of advantageous properties such as broad-spectrum activity, and they do not readily induce drug-resistance. However, AMPs have some intrinsic drawbacks, such as susceptibility to enzymatic degradation, toxicity, and high production cost. Currently, a new class of AMPs termed “peptidomimetics” have been developed, which can mimic the bactericidal mechanism of AMPs, while being stable to enzymatic degradation and displaying potent activity against multidrug-resistant bacteria. This review will focus on current findings of antimicrobial peptidomimetics. The potential future directions in the development of more potent analogs of peptidomimetics as a new generation of antimicrobial agents are also presented.

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“…Recently, a heterologous expression system has been constructed using small ubiquitin-related modifier-AGAP (SUMO-AGAP) which is a product of recombinant AGAP (rAGAP) linked with a hexa-histidine tag from Escherichia coli . This recombinant system showed considerable inhibition of lymphoma and glioma propagation (Gu et al, 2013). Using SW480 human colon cancer cells, it was proposed that rAGAP induces cell cycle arrest in the G0/G1 phase, attended by the decrease in the S phase without significant change in the G2/M phase (Gu et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Current scenario of peptide-based drugs: the key roles of cationic antitumor and antiviral peptides

et al. 2013

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Cationic antimicrobial peptides (AMPs) and host defense peptides (HDPs) show vast potential as peptide-based drugs. Great effort has been made in order to exploit their mechanisms of action, aiming to identify their targets as well as to enhance their activity and bioavailability. In this review, we will focus on both naturally occurring and designed antiviral and antitumor cationic peptides, including those here called promiscuous, in which multiple targets are associated with a single peptide structure. Emphasis will be given to their biochemical features, selectivity against extra targets, and molecular mechanisms. Peptides which possess antitumor activity against different cancer cell lines will be discussed, as well as peptides which inhibit virus replication, focusing on their applications for human health, animal health and agriculture, and their potential as new therapeutic drugs. Moreover, the current scenario for production and the use of nanotechnology as delivery tool for both classes of cationic peptides, as well as the perspectives on improving them is considered.

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Analgesic-antitumor peptide induces apoptosis and inhibits the proliferation of SW480 human colon cancer cells

Cited by 33 publications

References 40 publications

Genistein induces activation of the mitochondrial apoptosis pathway by inhibiting phosphorylation of Akt in colorectal cancer cells

Genistein induces activation of the mitochondrial apoptosis pathway by inhibiting phosphorylation of Akt in colorectal cancer cells

Peptidomimetics as a new generation of antimicrobial agents: current progress

Current scenario of peptide-based drugs: the key roles of cationic antitumor and antiviral peptides

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