beta-elemene and Carcinoma--Squamous-Cell

beta-elemene has been researched along with Carcinoma--Squamous-Cell* in 3 studies

Other Studies

3 other study(ies) available for beta-elemene and Carcinoma--Squamous-Cell

ArticleYear
Synergistic Cytotoxicity of β-Elemene and Cisplatin in Gingival Squamous Cell Carcinoma by Inhibition of STAT3 Signaling Pathway.
    Medical science monitor : international medical journal of experimental and clinical research, 2017, Mar-29, Volume: 23

    BACKGROUND Cisplatin remains one of the most active agents and is the mainstay of combination chemotherapy regimens against gingival squamous cell carcinoma. However, the efficacy of cisplatin is limited by its high toxicity and the development of drug resistance. β-elemene, isolated from the Chinese herb Rhizoma zedoariahas, is highly effective against malignancies and has low toxicity, but the development of β-elemene sensitizing chemotherapy in targeting the STAT3 signaling pathway remains unexplored in gingival squamous cell carcinoma. The present study was conducted to assess the chemosensitizing effects of b-elemene for enhancing the cytotoxicity of cisplatin in gingival squamous cell carcinoma. MATERIAL AND METHODS The gingival squamous cell carcinoma YD-38 cell line was used. MTT assay, clonogenic assay, annexin V/PI apoptosis assay, Western blot analysis, and xenograft model treatment were carried out in vitro and in vivo. RESULTS β-elemene significantly enhanced proliferative inhibition and cisplatin induced apoptosis in gingival squamous cell carcinoma. Cisplatin combined with β-elemene decreased the expressions of p-STAT3, p-JAK2, and Bcl-2, and increased the expressions of Bax and caspase-3 significantly compared to cisplatin only treatment, as well as in the xenograft model. CONCLUSIONS The results indicated that β-elemene promoted the anti-proliferative and apoptotic effect of cisplatin by inhibiting STAT3 and blocking the JAK2-STAT3 signaling pathway in GSCC in vitro and in vivo.

    Topics: Animals; Antineoplastic Agents; Apoptosis; Carcinoma, Squamous Cell; Cell Line, Tumor; Cell Proliferation; Cisplatin; Dose-Response Relationship, Drug; Drug Synergism; Gingival Neoplasms; Mice; Sesquiterpenes; Signal Transduction; STAT3 Transcription Factor; Xenograft Model Antitumor Assays

2017
Beta-elemene treatment is associated with improved outcomes of patients with esophageal squamous cell carcinoma.
    Surgical oncology, 2017, Volume: 26, Issue:4

    To investigate the therapeutic effects of concurrent preoperative β-elemene treatment in patients with esophageal squamous cell carcinoma who received concurrent chemoradiotherpay followed by surgery.. The clinicopathological parameters and outcomes of 102 patients with esophageal squamous cell carcinoma were studied and compared between patients treated with and without β-elemene.. β-elemene treatment could prolong the overall survival and progression-free survival. The 3-year overall survival rate was also increased by β-elemene treatment. β-elemene treatment was an independent prognostic factor for both overall survival and progression-free survival. Occurrence of toxicities associated with chemoradiotherapy was decreased by β-elemene treatment.. Findings in this study suggested that β-elemene treatment provided survival benefits and reduced chemoradiotherapy-associated toxicities in patients with esophageal squamous cell carcinoma.

    Topics: Adult; Aged; Carcinoma, Squamous Cell; Chemoradiotherapy; Esophageal Neoplasms; Female; Follow-Up Studies; Humans; Male; Middle Aged; Prognosis; Sesquiterpenes; Survival Rate

2017
β-Elemene inhibits the proliferation of esophageal squamous cell carcinoma by regulating long noncoding RNA-mediated inhibition of hTERT expression.
    Anti-cancer drugs, 2015, Volume: 26, Issue:5

    The study aimed to clarify the relationship between β-elemene, a long noncoding RNA (lncRNA), and human telomerase reverse transcriptase (hTERT) in esophageal carcinoma ECA-109 cells. The proliferation of ECA-109 cells was measured using a CCK-8 kit and flow cytometry. PCR microarray and real-time RT-PCR were designed to determine lncRNA expression in ECA-109 cells before and after treatment with β-elemene. Western blot was used to detect the hTERT level after the differentially expressed lncRNAs in ECA-109 cells were interfered with small interfering RNA (siRNA). On treatment with β-elemene, the proliferation of ECA-109 cells was notably inhibited, and about 85% of the lncRNAs showed higher expression levels in ECA-109 cells than in those untreated cells, from which, CDKN2B-AS1 was screened out. A specific siRNA (si-CDKN2B-AS1) that targets the β-elemene-mediated lncRNA CDKN2B-AS1 was designed, synthesized, and applied to treat ECA-109 cells. Its interference efficiency reached as high as 89.6%. When ECA-109 cells were transfected with the siRNA, the hTERT level was increased by 84.7%. The CCK-8 assay showed that the proliferation of ECA-109 cells treated with β-elemene was significantly promoted after siRNA transfection (P<0.01). It was also shown by flow cytometry that, compared with the scramble-treated group (negative control), the proliferation index value of ECA-109 cells in the si-CDKN2B-AS1 treatment group was notably increased (25.7 vs. 51.7%) and the TERT protein level was increased by 67.25% after the cells were treated with si-CDKN2B-AS1. The chemotherapeutic drug β-elemene suppressed the proliferation of esophageal carcinoma ECA-109 cells by regulating the inhibition of hTERT expression by lncRNA CDKN2B-AS1.

    Topics: Antineoplastic Agents; Carcinoma, Squamous Cell; Cell Line, Tumor; Cell Proliferation; Esophageal Neoplasms; Gene Expression Regulation; Humans; RNA, Long Noncoding; Sesquiterpenes; Telomerase

2015