Phytochemical constituents, in-vitro anticancer activity and computational studies of Cymbopogon schoenanthus.

The cytotoxic effects of Cymbopogon schoenanthus L. aerial part ethanol extract were examined against some cancer cell lines, and HUVEC normal cell lines using MTT assay. The ethanolic extract was prepared by ultrasonic-assisted extraction and analyzed by GC-MS and HPLC. The extract was found to be rich in terpene compounds. The extract proved to be highly selective and effective against breast and prostate cancer cell lines (MDA-MB-435, MCF-7, and DU 145) with IC50 as low as 0.7913 ± 0.14, 12.841 ± 0.21, and 30.51 ± 0.18 µg/ml, respectively. In silico modeling was performed to investigate the binding orientation and affinity of the major identified compounds against Polo-like kinase (PLK1 protein) a cancer molecular target using molecular docking and molecular dynamic whereas eudesm-5-en-11-ol, piperitone, and 2,3-dihydrobenzofuran displayed better binding affinity and stability against PLK1 compared to the reference drug. These findings encourage further in vivo studies to assess the anti-cancer effects of C. schoenanthus extract and its components.

[Corrigendum] In vitro and in vivo activities of an antitumor peptide HM-3: A special dose-efficacy relationship on an HCT­116 xenograft model in nude mice.

After the publication of the article, the authors have realized that Figs. 3 and 7 in their paper were published with errors; in the first instance, regarding Fig. 3, panels 'C' and 'D' contained partially overlapping data and were derived from the same original source, where these images were intended to show the effect of 2 ng/ml sunitinib and 2 µg/ml HM­3, respectively, on cell migration. Likewise, in Fig. 7, panels 'C' and 'D' also contained partially overlapping data derived from the same original source, even though these images were intended to show representative images for sections of tumor tissue from the HM­3 (3 mg/kg) and HM­3 (48 mg/kg) treatment groups. These errors arose inadvertently, as a consequence of the authors' mishandling of their data. The revised versions of Figs. 3 and 7, featuring the corrected data panels for panels 'C' and 'D' in both Figures, are shown opposite. The revised data shown for these Figures do not affect the overall conclusions reported in the paper. The authors apologize to the Editor of Oncology Reports and to the readership for any inconvenience caused. [the original article was published in Oncology Reports 36: 2951­2959, 2016; DOI: 10.3892/or.2016.5077].

In vitro and in vivo activities of an antitumor peptide HM-3: A special dose-efficacy relationship on an HCT­116 xenograft model in nude mice.

Anti-angiogenesis is an important therapy for cancer treatment. Peptide HM-3 is an integrin antagonist with anti-angiogenic and antitumor activity. Previous research found that HM-3 at an effective dose inhibited tumor growth whereas at higher doses, the inhibitory effect gradually decreased. In the present study, three human tumor cell lines, human colorectal cancer cell (HCT-116) and human hepatic cancer cell (Hep G-2 and SMMC-7721), were selected and their interactions with HM-3 were compared with western blot and flow cytometric assays. The effect of HM-3 on the migration of two tumor cell lines (HCT-116 and Hep G-2) was also evaluated and a bell-shaped dose-efficacy curve was found for both cell lines. Furthermore, in vivo imaging in BALB/c nude mice confirmed that HM-3 had a short half-life and targeted the tumor tissue. Moreover, on an HCT-116 xenograft model in BALB/c nude mice, HM-3 at 3 mg/kg inhibited tumor growth with an inhibition rate of 71.5% (by tumor mass) whereas at 12 and 48 mg/kg, the inhibition rates were 59.2 and 36.0%, respectively. Immunohistochemistry analyses found that both sunitinib (60 mg/kg) and HM-3 (3 and 48 mg/kg) decreased microvascular density and increased percent of HIF-1α and VEGF expressing cells. The present study investigated the effect of tumor microenvironments on the antitumor effect of HM-3 and concluded that HM-3 inhibited angiogenesis and thereafter tumor growth by directly inhibiting HUVEC migration. The special dose-efficacy curves for antitumor effect and for cell migration inhibition were correlated. The present study also confirmed that the effective dose has to be strictly defined for better clinical applications of anti­angiogenic drugs such as HM-3.