AO/EB staining of cancer cells showed that gammacerane is active in inducing apoptosis in RL-95 cells and apoptotic induction effects were more evident at higher concentrations of the molecule. Flow cytometric analysis with Annexin V-FITC/Propidium iodide (PI) fixed cells showed that the percentage of apoptotic cells increased with increase in gammacerane concentration. Apoptotic signal was mediated via the modulation of Bax/Bcl-2 protein ratio. Western blot analysis of STAT3 protein showed that gammacerane treatment reduced the protein levels of STAT3 and the effects were more prominent at higher treatment concentrations. Conclusion Gammacerane, by its ability to take control over the transcription of STAT3 transcription factor, inhibits the proliferation of human endometrial cancer cells. The effects revealed loss of viability, arrest of mitosis and cellular apoptosis.Purpose A good number of anticancer studies have focused on the evaluation of plant derived natural products against different types of human cancers. Triterpenes, belonging to terpenoid class of plant secondary metabolites, have been reported to function as potent anticancer agents. The current study was designed to investigate the anticancer potential of Taraxastane against human cervical cancer cells. Methods MTT assay and DAPI staining were used for determining the cell viability. DCFH-DA and DiOC6 based estimations were employed for determination of reactive oxygen species (ROS) and mitochondrial membrane potential (MMP), respectively. Flow cytometry technique was used for analysis of cell cycle and necrosis. read more Analysis of cell migration and invasion was performed by wound heal and transwell assays, repectively. Protein expression was analyzed by Western blotting. Results MTT assay showed that Taraxastane inhibited the proliferation of DoTc2 cervical cancer cells in a concentration-dependent manner with antane has remarkable anti- proliferative effect on human cervical cancer cells and thus may prove as a vital lead molecule for discovery of anticancer drugs.Purpose This study was designed to examine the in vitro and in vivo antitumor effects of Cinnamolide against cisplatin-resistant human cervical cancer cells (HeLa cells). Methods Cell viability was examined by WST-1 cell viability assay. Cinnamolide-induced apoptosis was examined by fluorescent microscopy using acridine orange (ΑΟ) /ethidium bromide (EB) staining and flow cytometry in combination with annexin-V/propidium iodide (PI) staining. Western blot was used to study the effects of Cinnamolide on apoptosis-related protein expressions including Bax and Bcl-2 as well as to study effects on numerous caspases and Akt/β-Catenin signaling pathway. Effects on mitochondrial membrane potential (MMP) were evaluated by flow cytometry. In vivo studies using xenograft mouse model were carried out to evaluate the efficacy of Cinnamolide under in vivo conditions. Results Cinnamolide decreased the viability of the HeLa human cervical cancer cells and exhibited an IC50 of 16.5 µM. The cytoxicity of Cinnamolide was also indicate that Cinnamolide natural product has the potential to be developed as a promising anticancer agent against human cervical carcinoma.Purpose Triple-negative breast cancer (TNBC) is one of the most ordinary malignant tumors. Recent studies have revealed that long noncoding RNAs (lncRNAs) play an important role in the progression of tumorigenesis. This study aimed to identify how lncRNA DGCR5 functions in the progression of TNBC. Methods DGCR5 expression of both 57 paired TNBC patients' tissue samples and cells was detected by real-time quantitative polymerase chain reaction (RT-qPCR). Moreover, the function of SNHG7 was identified by performing proliferation assay and transwell assay in vitro. Besides, the underlying mechanism was explored through Western blot assay and RT-qPCR. In addition, tumor formation and metastasis assays were also conducted in vivo. Results In this study, DGCR5 expression was obviously higher in TNBC tissues when compared with that in adjacent non-tumor samples. Cell proliferation, migration and invasion in TNBC were inhibited after knockdown of DGCR5 in vitro. Moreover, results of further experiments revealed that the targeted proteins in Wnt/β-catenin signaling pathway were downregulated via knockdown of DGCR5 in TNBC. Furthermore, tumor formation and metastasis of TNBC were inhibited via knockdown of DGCR5 in nude mice. Conclusions Our study suggests that DGCR5 enhances TNBC cell proliferation and metastasis via inducing Wnt/β-catenin signaling pathway in vitro and in vivo.Purpose Studies have shown that α-enolase ENO1 is involved in the regulation of cancer cell proliferation and metastasis. However, the role of ENO1 is yet to be explored in breast cancer. This study was undertaken to explore the role and therapeutic potential of ENO1 in breast cancer. Methods Expression analysis was carried out by qRT-PCR. Transfections were performed by Lipofectamine 2000 reagent. WST-1 assay was used for cell viability. Wound healing assay was used for cell migration analysis. Western blot analysis was used to determine protein expression. Results The results showed that the expression of ENO1 was significantly upregulated in breast cancer by up to 4-fold. Silencing of ENO1 caused significant decline in the proliferation rate and colony formation of the SK-BR-3 breast cancer cells. The decrease in the proliferation rate of the ENO1 cells was due to the induction of apoptosis as revealed by DAPI staining. Annexin V/propidium iodide (PI) showed a significant increase in the apoptotic SK-BR-3 cells. The apoptosis percentage was 2.17 in si-NC and 23.1% in si-ENO1 transfected SK-BR-3 cells. The apoptosis induction was also accompanied by increase in Bax and decrease in Bcl-2 expression. ENO1 silencing also resulted in the arrest of the SK-BR-3 cells in the G2/M phase of the cell cycle which was also associated with depletion of Cdc2, Cdc25 and cyclin B1 expression levels. ENO1 silencing also caused decrease in the migration and invasion of the SK-BR-3 cells as revealed by the wound healing and transwell assays. Conclusion These findings suggest that ENO1 has oncogenic properties in breast cancer which can be exploited in breast cancer treatment.read more