Teresa Liliana Wargasetia

Mechanisms of cancer cell killing by sea cucumber-derived compounds

SummaryThe aim of cancer therapy is to specifically eradicate tumor cells while causing minimal damage to normal tissues and minimal side-effects. Because of this, the use of natural substances with low toxicity is a good option. Sea cucumbers are one of many potential marine animals that contain valuable nutrients and medicinal properties. The medicinal value of sea cucumbers is attributed to the presence of bioactive agents with promising biological and pharmacological properties that include cytotoxic activity, induction of apoptosis, cell cycle arrest, inhibition of tumor growth, anti-metastatic and anti-angiogenic properties, and inhibition of drug resistance. This review discusses the mechanisms of cancer cell death induced by sea cucumber-derived compounds with regard to exploring the potential use of these marine natural products for cancer therapy.

The Role of Sea Cucumber Active Compound and Its Derivative as an Anti-Cancer Agent

Purpose of ReviewThis article gives a brief overview on the role of sea cucumber active compounds in cancer cell killing that may be developed into a potent anti-cancer agent.Recent FindingsThe rapid development of knowledge and technology in molecular biology has as yet not succeeded in identifying a safe drug for cancer therapy. The central issue in cancer treatment is the side effects of the cancer medicines and the cancer cell resistance that develop against the drugs. An alternative medication is the use of natural materials as a substance for cancer treatment with fewer side effects. Sea cucumber is an edible marine animal that has been widely used for food and traditional medicine and has not been reported as toxic for humans. Further, we summarized the latest information on the sea cucumber research, its active compound, and its role in the cancer cell killing. The sea cucumber contains active compounds that can potentially be used as an anti-cancer agent that is safe for humans.SummaryThe sea cucumber contains active substances which are toxic to various cancer cells and can therefore function as an anti-cancer agent. Some studies have concluded that the active compounds display anti-metastasis and anti-angiogenesis activity. Moreover, the compounds also work to inhibit cell division and induce apoptosis both in vitro and in vivo. The particular role of sea cucumber as a potential anti-cancer agent has also been described in this review. Indeed, this article presents the latest information and concept of the cancer-killing mechanism of sea cucumber that warrants a significant further investigation into cancer mechanisms to identify a safe drug.

Potential use of compounds from sea cucumbers as MDM2 and CXCR4 inhibitors to control cancer cell growth

Ineffectiveness of cancer therapy may originate in the incompatibility of the treatment with various mutations in the cancer cells. Finding novel anticancer treatments that work efficiently for varying types of cancer cells remains challenging. Previous studies have identified that compounds in sea cucumbers are capable of inhibiting the growth of cancer cells and inducing apoptosis. However, information on the underlying mechanisms controlling cancer cell growth at a molecular level remains limited. The current study analyzed the potential of colochiroside A, ds-echinoside A, philinopside E, sphingosine and stichoposide C as inhibitors for anticancer target proteins, including mouse double minute 2 homolog (MDM2) and C-X-C chemokine receptor type 4 (CXCR4). Inhibition of MDM2 triggers apoptosis through regulation of tumor protein 53 and CXCR4 inhibition may prevent cancer cell proliferation and growth by affecting the Janus kinase 2/3 signal transducer and activator of transcription signaling pathway and protein tyrosine kinase 2. The results of a binding affinity analysis using molecular docking revealed that philinopside E and ds-echinoside A may inhibit MDM2 and CXCR4. The data suggested that these active compounds may be promising inhibitors of cell growth by binding to two targets simultaneously. Furthermore, stichoposide C and colochiroside A were predicted to inhibit CXCR4. Additional research is needed to validate the in vitro activity of the aforementioned compounds.

Upregulation of two human microRNAs which might be involved in the carcinogenesis of nasopharyngeal cancer and that are promising for biomarker development

One of the biggest problems in diagnosing nasopharyngeal carcinoma (NPC) is the lack of biomarkers to detect the disease in its early stages. Thus, the exploration of biomarkers, which have the potential to be used to diagnose NPC in its early stages, is crucial. NPC is allegedly controlled by microRNAs (miRNAs); these molecules can be secreted out of cells and can be found in the serum—two aspects that make them potential biomarkers to be developed for non-invasive diagnosis of NPC. In this study, we analyzed the profile of miRNA expression in NPC biopsy tissue compared to normal tissues. The miRNA expression is taken from 246 samples of patients with NPC, compared to 17 samples from non-NPC subjects as the control. The results of the analysis identified more than 100 miRNAs that underwent an upregulation of expression in NPCs compared to that in the control group. Further analysis was focused on understanding the role of the miRNAs that were upregulated in NPCs. The results of this analysis reveal that there are six miRNAs: hsa-miR-1246, hsa-miR-320a, hsa-miR-1290, hsa-miR-146b-5p, hsa-miR-107, and hsa-miR-1305, which underwent increased expression and that are closely related to process of cancer (carcinogenesis) in NPC. Among the upregulated miRNA, the two miRNAs, miR-1290 and miR-1246, were found upregulated in the serum of NPC patients compared to the health persons. Moreover, the target genes of the miRNAs are also targets of the oncovirus protein that is involved in controlling the cell cycle and apoptosis. Upregulation of the miRNA might stimulate carcinogenesis through repressing guard genes for controlling cell cycle and apoptosis. The mechanism seems similar to the way the oncovirus initiates cancer.