Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0029463 (osteosarcoma)
 16,637 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A novel microRNA, miR-520d-5p, can inhibit proliferation of osteosarcoma cells, but the biological role of miR-520d-5p in lung cancer is notknown. Midazolam can induce apoptosis in many kinds of cancer cells, but there are no reportson its use in lung cancer. We investigated the roles of midazolam and miR-520d-5p in apoptosis induction in a non-small cell lung cancer (NSCLC) cell line (A549). The expression of miR-520d-5p, a signal transducer and activator of transcription 3 (STAT3) and its related protein were measured by quantitative real-time PCR and Western blot. Apoptosis of the NSCLC cells in response to midazolam was determined by MTT assay, flow cytometry, and Western blot. Midazolam significantly induced A549 cell apoptosis and modulated expression of Bcl-2, Bax, and Caspase-3. Additionally, midazolam regulated STAT3 expression in A549 cells, and the siRNA inhibited STAT3 levels, highlighting their roles in the regulation of STAT3 signaling. Midazolam combined with the miR-520d-5p mimic and inhibitor, regulated STAT3 expression and its signaling pathway. Midazolam combined with the miR-520d-5p mimic significantly induced A549 cell apoptosis. Thus, midazolam can induce apoptosis of A549 cells by targeting STAT3 via miR-520d-5p. These findings suggest that midazolam might be a putative anti-cancer approach for NSCLC therapy.
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PMID:Midazolam induces A549 cell apoptosis in vitro via the miR-520d-5p/STAT3 pathway. 3193 32

Disrupted centrosome-associated family protein expression can result in the detrimental duplication of centrosomes, causing genomic instability and subsequent carcinogenesis. Limited research has demonstrated that centrosomal protein 131 (CEP131) exhibits oncogenic activity in osteosarcoma, hepatocellular carcinoma and breast cancer. The present study demonstrated that there is an association between CEP131 expression and advanced Tumor-Node-Metastasis stage (P=0.016), and positive regional lymph node metastasis (P=0.023) in 91 cases of non-small cell lung cancer. A549 and SPC-A-1 cells, with moderate expression levels of CEP131, were selected as representative cell lines. The results indicated that downregulation of CEP131 induced G1/S cell cycle arrest, inhibition of cyclins D1/E and cyclin-dependent kinases 2/4/6, and induction of inhibitory p21/p27, all of which are regulated by ERK and AKT signaling, suggesting that CEP131 exhibits potential as a novel target in the treatment of lung cancer.
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PMID:CEP131 knockdown inhibits cell proliferation by inhibiting the ERK and AKT signaling pathways in non-small cell lung cancer. 3221 65

Long noncoding RNA (lncRNA) is a newly identified type of noncoding RNA with a length of more than 200 nucleotides. The latest research shows that lncRNAs play important roles in the occurrence and development of human tumours by acting both as carcinogenic genes and as tumour suppressor genes. LncRNAs plays a role in various biological processes, such as cell growth, apoptosis, migration and invasion. The newly discovered lncRNA DDX11-AS1 is abnormally highly expressed in various malignant tumours, such as hepatocellular carcinoma, colorectal cancer, osteosarcoma, bladder cancer, NSCLC and gastric cancer. DDX11-AS1 mainly regulates the expression of related genes through direct or indirect ways to perform its functions in carcinogenicity. These results indicate that DDX11-AS1 may be a marker or therapeutic target of tumours. This review summarizes the biological function and mechanism of DDX11-AS1 in the process of tumour development.
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PMID:LncRNA DDX11-AS1: a novel oncogene in human cancer. 3277 30

Over the past decade, a number of studies have demonstrated the resistance of cancer cells to conventional drugs and have recognized this as a major challenge in cancer therapy. While attempting to understand the underlying mechanisms of chemoresistance, several studies have suggested that the presence of cancer stem cells (CSCs) in tumors is one of the major pathways contributing toward resistance. Chemoresistance leads to cancer treatment failure and worsens the prognosis of patients. Natural herbal compounds are gaining attention as an alternative treatment strategy for cancer. These compounds may be effective against chemoresistant cells either alone or synergistically alongside conventional drugs, sensitizing cancer cells and enhancing the therapeutic efficacy. BRM270 is a natural compound made from seven herbal plant (Saururus chinensis, Citrus unshiu Markovich, Aloe vera, Arnebia euchroma, Portulaca oleracea, Prunella vulgaris var. lilacina and Scutellaria bacicalensis) extracts used in Asian traditional medicine and has the potential to target CSCs. Several studies have demonstrated the positive effects of BRM270 against chemoresistant cancer and its synergy alongside existing cancer drugs, including paclitaxel and gefitinib. These effects have been observed against various cancer types, including resistant non-small cell lung cancer (NSCLC), glioblastoma, multi-drug resistant osteosarcoma, cervical cancer, pancreatic cancer and hepatocarcinoma. The present review discusses the effects of BRM270 treatment against CSC-associated chemoresistance in common types of cancer.
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PMID:BRM270 targets cancer stem cells and augments chemo-sensitivity in cancer. 3283 22

Following the discovery of cisplatin over 50 years ago, platinum-based drugs have been a widely used and effective form of cancer therapy, primarily causing cell death by inducing DNA damage and triggering apoptosis. However, the dose-limiting toxicity of these drugs has led to the development of second and third generation platinum-based drugs that maintain the cytotoxicity of cisplatin but have a more acceptable side-effect profile. In addition to the creation of new analogs, tumor delivery systems such as liposome encapsulated platinum drugs have been developed and are currently in clinical trials. In this study, we have created the first PEGylated liposomal form of nedaplatin using thin film hydration. Nedaplatin, the main focus of this study, has been exclusively used in Japan for the treatment of non-small cell lung cancer, head and neck, esophageal, bladder, ovarian and cervical cancer. Here, we investigate the cytotoxic and genotoxic effects of free and liposomal nedaplatin on the human non-small cell lung cancer cell line A549 and human osteosarcoma cell line U2OS. We use a variety of assays including ICP MS and the highly sensitive histone H2AX assay to assess drug internalization and to quantify DNA damage induction. Strikingly, we show that by encapsulating nedaplatin in PEGylated liposomes, the platinum uptake cytotoxicity and genotoxicity of nedaplatin was significantly enhanced in both cancer cell lines. Moreover, the enhanced platinum uptake as well as the cytotoxic/antiproliferative effect of liposomal nedaplatin appears to be selective to cancer cells as it was not observed on two noncancer cell lines. This is the first study to develop PEGylated liposomal nedaplatin and to demonstrate the superior cell delivery potential of this product.
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PMID:Encapsulation of Nedaplatin in Novel PEGylated Liposomes Increases Its Cytotoxicity and Genotoxicity against A549 and U2OS Human Cancer Cells. 3292 97

Osteosarcoma (OS) is a type of primary bone tumor, which is one of the leading causes of cancer-related death. MicroRNA (miR)-605 has been demonstrated to act as a prognostic biomarker and therapeutic target in various cancers, such as breast cancer and non-small cell lung cancer, but its function in OS remains unclear. The aim of the present study was to investigate the prognostic value of miR-605 in patients with OS by evaluating its expression levels and to explore the biological function of miR-605 in OS progression. For this purpose, tumor tissues and adjacent normal tissues were collected from OS patients, and the expression of miR-605 in the collected tissues and OS MG63, U2OS, HOS, and SAOS-2 cell lines was detected by quantitative real-time PCR. The prognostic value of miR-605 was evaluated by Kaplan-Meier survival curves and Cox regression analysis. The effects of miR-605 on OS cell proliferation, migration and invasion were analyzed by the CCK-8 and transwell assays, respectively. The results of the present study revealed that miR-605 was significantly downregulated in OS tissues compared with adjacent normal tissues, which was associated with the clinical stage and distant metastasis of patients. Additionally, the downregulation of miR-605 predicted the poor prognosis of patients with OS and served as an independent prognostic indicator. The downregulation of miR-605 enhanced cell proliferation, migration, and invasion of OS cells, which suggested that miR-605 may be involved in the progression of OS. The findings of the present study provide a new therapeutic target for the treatment of patients with OS.
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PMID:Downregulation of microRNA-605 indicates poor prognosis and promotes the progression of osteosarcoma. 3315 68


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