Cecropin‐P17, an analog of Cecropin B, inhibits human hepatocellular carcinoma cell HepG‐2 proliferation via regulation of ROS, Caspase, Bax, and Bcl‐2

Wu, Chunli; Geng, Xiaoping; Wan, Shengyun; Hou, Hui; Yu, Fanzong; Jia, Benli; Wang, Lei

doi:10.1002/psc.2786

Cited by 16 publications

(16 citation statements)

References 27 publications

(30 reference statements)

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“…Increased Bax expression can prolong the patients’ survival in ovarian cancer [27, 28]. Cecropin-P17 significantly suppresses hepatic tumor growth in vivo by stimulating BAX and inhibition Bcl-2 expression [29]. The in vivo and in vitro binding assay proved that ZNF667 can directly bind to the Bax promoter [12].…”

Section: Discussionmentioning

confidence: 99%

ZNF667 Serves as a Putative Oncogene in Human Hepatocellular Carcinoma

Cheng

Chen²,

Zhao

et al. 2017

Cell Physiol Biochem

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Background/Aims: Zinc finger protein 667 (ZNF667) is a member of C2H2 zinc finger protein family. For the first time, we aim to analyze the expression pattern of ZNF667 in hepatocellular carcinoma (HCC) tissues; to explore its role in HCC tumorigenesis. Methods: Immuno-histochemistry was carried out to characterize the ZNF667 expression in paraffin-embedded HCC samples. The relationship between ZNF667 expression and the clinical, pathological data of the patients were analyzed. Human normal hepatocyte cells LO2 over expressing ZNF667 (LO2-ZNF667 cells), ZNF667 depleted hepatocellular carcinoma HepG2 cells (HepG2-shZNF667 cells) were set up, their proliferation, migration and invasion abilities were analyzed. Xenograft nude mice were used to analyze the malignancy of HepG2-shZNF667 cells in vivo. Western blot was performed to analyze the expression of Bcl-2 and BAX in LO2-ZNF667 and HepG2-shZNF667 cells. Results: Increased ZNF667 was found via immuno-histochemistry in HCC. Enhanced ZNF667 expression was associated with tumor size, clinical stage and tumor differentiation. LO2-ZNF667 cells displayed increased and HepG2-shZNF667 cells decreased cell proliferation, migration and invasion. Xenograft experiments proved reduced malignancy of HepG2-shZNF667 cells in vivo. LO2-ZNF667 cells displayed increased Bcl-2 and decreased BAX protein expression. HepG2-shZNF667 cells displayed enhanced BAX and inhibited BCL-2 expression. Conclusions: ZNF667 is shown to be a new oncogene in HCC and it may serve as a new therapeutic target for HCC via enhancing BCL-2 and decreasing BAX expression.

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Section: Discussionmentioning

confidence: 99%

ZNF667 Serves as a Putative Oncogene in Human Hepatocellular Carcinoma

Cheng

Chen²,

Zhao

et al. 2017

Cell Physiol Biochem

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“…Interestingly, Choi and Lee (2013) showed that when the first six amino acid residues (GWGSFF) of pleurocidin (Table 2) were truncated, the peptide lost its effect on ROS production (apoptosis), apparently because the N-terminus of pleurocidin contains a BH3-like motif (Table 2, underlined amino acids). Similarly, cecropin-P17 (Table 2) was shown to suppress the proliferation of HepG-2 cells by inducing apoptosis, which was dependent (among other things) on inhibiting Bcl-2 (Wu et al, 2015).…”

Section: Resultsmentioning

confidence: 97%

Novel anionic cecropins from the spruce budworm feature a poly-L-aspartic acid C-terminus

Maaroufi

Cusson

Levesque

2018

Preprint

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19Cecropins form a family of amphipathic α-helical cationic peptides with broad-spectrum 20 antibacterial properties and potent anticancer activity. The emergence of bacteria and 21 cancer cells showing resistance to cationic antimicrobial peptides (CAMPs) has fostered 22 a search for new, more selective and more effective alternatives to CAMPs. With this 23 goal in mind, we looked for cecropin homologs in the genome and transcriptome of the 24 spruce budworm, Choristoneura fumiferana. Not only did we find paralogs of the 25 conventional cationic cecropins (Cfcec + ), our screening also led to the identification of 26 previously uncharacterized anionic cecropins (Cfcec -), featuring a poly-L-aspartic acid 27 C-terminus. Comparative peptide analysis indicated that the C-terminal helix of Cfcecis 28 amphipathic, unlike that of Cfcec + , which is hydrophobic. Interestingly, molecular 29 dynamics simulations pointed to the lower conformational flexibility of Cfcecpeptides, 30 relative to that of Cfcec + . Phylogenetic analysis suggests that the evolution of distinct 31 Cfcec + and Cfcecpeptides may have resulted from an ancient duplication event within 32 the Lepidoptera. Our analyses also indicated that Cfcecshares characteristics with 33 entericidins, which are involved in bacterial programmed cell death, lunasin, a peptide of 34 plant origins with antimitotic effects, and APC15, a subunit of the anaphase-promoting 35 complex. Finally, we found that both anionic and cationic cecropins contain a BH3-like 36 motif (G-[KQR]-[HKQNR]-[IV]-[KQR]) that could interact with Bcl-2, a protein 37 involved in apoptosis; this observation is congruent with previous reports indicating that 38 cecropins induce apoptosis. Altogether, our observations suggest that cecropins may 39 provide templates for the development of new anticancer drugs. 40 41 42 acid; ancient duplication; apoptotic motif; anticancer peptide. 43 44 45 3 Graphical abstract 46 47 48 Highlights 50

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“…The effects of TT-1 on the activity of caspase-3 and -9 in TT cells were determined using a fluorometric assay kit (Calbiochem; EMD Millipore) according to the manufacturer's protocol as previously described (24). Briefly, TT cells were treated with TT-1 (0-8 µg/ml) for 48 h and harvested prior to the preparation of cell lysates.…”

Section: Western Blot Analysis For Bax and Bcl-2 Protein Expressionmentioning

confidence: 99%

TT‑1, an analog of melittin, triggers apoptosis in human thyroid cancer TT cells via regulating caspase, Bcl‑2 and Bax

Wan

Zhang

et al. 2017

Oncol Lett

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Abstract. Melittin is a 26 amino acid residue antimicrobial peptide with known antitumor activity. In the present study, a novel peptide TT-1, derived from melittin and contained only 11 amino acids, was designed, and its antitumor effect was investigated. The present study is aimed to elucidate the effects and relative mechanisms of TT-1 on a human thyroid cancer cell line (TT) in vitro and in vivo. Cell viability assays, Annexin V/propidium iodide assays, western blotting and quantitative reverse transcription polymerase chain reaction were performed. Furthermore, a tumor-xenograft model was established to investigate the apoptotic mechanisms of TT-1 on TT cells. The results obtained indicated that TT-1 was able to suppress the proliferation of TT cells and exhibited low cytotoxicity to normal thyroid cells in vitro. The apoptotic rates of TT cells were also increased following TT-1 treatment. Additionally, TT-1 stimulated caspase-3, caspase-9 and Bax, and inhibited B-cell lymphoma 2 mRNA and protein expression. Finally, it was also demonstrated that TT-1 is able to markedly suppress tumor growth in a TT-bearing nude mouse model. In summary, TT-1 may inhibit the proliferation of TT cells by inducing apoptosis in vitro and in vivo, indicating that TT-1 may be a potential candidate for the treatment of thyroid cancer.

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Cecropin‐P17, an analog of Cecropin B, inhibits human hepatocellular carcinoma cell HepG‐2 proliferation via regulation of ROS, Caspase, Bax, and Bcl‐2

Cited by 16 publications

References 27 publications

ZNF667 Serves as a Putative Oncogene in Human Hepatocellular Carcinoma

ZNF667 Serves as a Putative Oncogene in Human Hepatocellular Carcinoma

Novel anionic cecropins from the spruce budworm feature a poly-L-aspartic acid C-terminus

TT‑1, an analog of melittin, triggers apoptosis in human thyroid cancer TT cells via regulating caspase, Bcl‑2 and Bax

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