Aim To study the inhibitory and apoptosis-inducing effects of aspisol on proliferation of B16 melanoma in vitro and in vivo. Methods The effect of aspisol on the proliferation of B16 cells was analyzed by MTT assay; its effect on cell apoptosis was measured by flow cytometry. The suspension of melanoma cells was injected subcutaneously into forelimb axillas of C57BL/6J mice to establish xenograft models. From the next day, the mice received intraperitoneal injection of aspisol in different concentrations once a day for 28 days; the mice received injection of dacarbazine (DTIC) were used as positive controls,and received injection of normal saline (NS) were used as negative controls. The inhibition rate of tumor growth was calculated .The apoptosis rate was detected by TUNEL assay. The expression of Survivin and C-erbB-2 was detected by immunohistochemistry. Results Aspisol inhibited the proliferation of B16 cells, with the inhibition rate up to (68.78?1.27)%, and induced the apoptosis with the highest apoptosis rate up to 15.8%.The inhibition rate of tumor growth was 15.0% in 200 mg?kg-1 aspisol group, 32.3% in 400 mg?kg-1 aspisol group, 49.4% in 800 mg?kg-1 aspisol group,and 51.4% in 40 mg?kg-1 DTIC group. Typical apoptotic morphologic changes were seen in the 4 groups. Survivin and C-erbB-2 expression was significantly lower in aspisol groups than in NS group. Conclusion Aspisol could inhibit proliferation and induce apoptosis of B16 melanoma cells in vitro and in vivo, which may be correlated to down-regulation of Survivin and C-erbB-2.

Background and purpose:Many studies indicate that nonsteroidal anti-inflammatory drugs(NSAIDs) may inhibit cancer growth.However,the molecular mechanisms may involve different pathway and still remain unclear.The aim of this experiment was to investigate the influence of aspisol against breast cancer lines,including MDA-MB-231(estrogen receptor-negative),MCF-7(estrogen receptor-positive),and reveal the potential signaling pathway mechanism of aspisol effect on breast cancer lines.Methods:MDA-MB-231 and MCF-7 human breast cancer cell lines were treated with aspisol in vitro.Cell proliferation was evaluated by MTT assay and rate of apoptosis were determined by flow cytometry.Extracellular signal regulated kinase(ERK),phosphor-ERK(P-ERK) protein expressed in breast cancer cell lines were analyzed by Western blot.Results:①The results of MTT assay demonstrated that the growth of MDA-MB-231,MCF-7 cells were inhibited by aspisol in a time-and dose-dependent fashion(P0.05).Conclusions:aspisol inhibits proliferation and induces apoptosis not only in ER-positive but also in ER-negative breast cancer cells.The mechanism may relate to ERK signal pathway.

AIM: To investigate the expression of microRNA-625-3p ( miR-625-3p) in colorectal carcinoma ( CRC) and its underlying mechanism .METHODS:Quantitative real-time PCR was employed to detect the levels of miR-625-3p expression in different CRC cell lines , CRC tissues and pair-matched adjacent normal tissues .The relationships be-tween the expression levels of miR-625-3p and the patients’clinicopathological parameters were estimated .The effects of miR-625-3p on the apoptosis and the cell mitotic cycle of CRC cells were analyzed with propidium iodide staining and flow cytometry.The effect of miR-625-3p on the apoptosis-related proteins was analyzed by Western blot .RESULTS: The ex-pression level of miR-625-3p in the CRC tissues was higher than that in the pair-matched adjacent normal tissues ( P <0.05).The expression of miR-625-3p in the CRC tumor tissues was significantly correlated with the tumor infiltrative depth , TNM stage and distant metastasis (P<0.05).The expression levels of miR-625-3p in CRC SW620 cells were higher than that in SW480 cells.The CRC cell mitotic cycle was significantly inhibited and cell apoptosis was significantly promoted when the expression of miR-625-3p was inhibited (P<0.05).The expression of Bax protein didn’t change and the expres-sion of Bcl-2 protein increased after miR-625-3p mimics were transfected into CRC SW620 cells(P<0.05).CONCLU-SION:miR-625-3p may be a promising approach for the treatment of CRC by promoting cell proliferation and inhibiting apoptosis .

Substantial progress in the use of chemo-photodynamic nano-drug delivery systems (nano-DDS) for the treatment of the malignant breast cancer has been achieved. The inability to customize precise nanostructures, however, has limited the therapeutic efficacy of the prepared nano-DDS to date. Here, we report a structurally defined tandem-responsive chemo-photosensitive co-nanoassembly to eliminate primary breast tumor and prevent lung metastasis. This both-in-one co-nanoassembly is prepared by assembling a biocompatible photosensitive derivative (pheophorbide-diphenylalanine peptide, PPA-DA) with a hypoxia-activated camptothecin (CPT) prodrug [(4-nitrophenyl) formate camptothecin, N-CPT]. According to computational simulations, the co-assembly nanostructure is not the classical core-shell type, but consists of many small microphase regions. Upon exposure to a 660 nm laser, PPA-DA induce high levels of ROS production to effectively achieve the apoptosis of normoxic cancer cells. Subsequently, the hypoxia-activated N-CPT and CPT spatially penetrate deep into the hypoxic region of the tumor and suppress hypoxia-induced tumor metastasis. Benefiting from the rational design of the chemo-photodynamic both-in-one nano-DDS, these nanomedicines exhibit a promising potential in the inhibition of difficult-to-treat breast tumor metastasis in patients with breast cancer.