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A new γ-lactone compound, trichonafurin A (1), was obtained from the culture of Trichoderma atroviride ZW-7, an endophyte of the marine brown alga Sargassum thunbergii. Its structure was unambiguously assigned by detailed interpretation of 1D/2D NMR and HRESIMS data. Trichonafurin A (1) exhibited moderate cytotoxicity against HeLa and HepG2 cell lines with IC50 values of 20.2 and 32.1 μM, respectively. [ABSTRACT FROM AUTHOR]

A new carotane sesquiterpene, trichocarotin N (1), was isolated from a culture of the marine-derived fungus Trichoderma virens QD-11. The structure of this compound was established by detailed analysis of 1D/2D NMR and HRESIMS data. Trichocarotin N (1) exhibited moderate cytotoxicity against HeLa and MCF-7 cancer cell lines, with IC50 values of 32.4 and 41.6 μM, respectively. A new carotane sesquiterpene, trichocarotin N (1), was isolated from a culture of the marine-derived fungus Trichoderma virens QD-11. The structure of this compound was established by detailed analysis of 1D/2D NMR and HRESIMS data. Trichocarotin N (1) exhibited moderate cytotoxicity against HeLa and MCF-7 cancer cell lines, with IC50 values of 32.4 and 41.6 μM, respectively. [ABSTRACT FROM AUTHOR]

A new norsesquiterpene and four known bisabolanes were obtained from the organic extract of Trichoderma atroviride TD-8 isolated from ocean sediments. Their structures were assigned by detailed interpretation of 1D/2D NMR and HRESIMS data, and they were determined to be nor-bisabolan-1,11-diol (1), (3R,6R,7R)-1,10-bisaboladien-3-ol (2), (3R,6R,7S)-1,10-bisaboladien-3,6-diol (3), (3R,6S,7R,10R)-1-bisabolen3,10,11-triol (4), (3R,6R,7S,10R)-1-bisabolen-3,10,11-triol (5). Nor-bisabolan-1,11-diol (1) exhibited moderate cytotoxicity against HeLa and HCT-8 cell lines with IC50 values of 28.6 and 30.3 μM, respectively. [ABSTRACT FROM AUTHOR]

Activity-guided isolation of the fermentation broth of the deep-sea derived fungus Acaromyces ingoldii FS121, which was obtained from the China South Sea, yielded a new naphtha-[2,3-b]pyrandione analogue, acaromycin A (1) and a new thiazole analogue, acaromyester A (2), as well as the known compound (+)-cryptosporin (3). Their structures, including absolute configurations, were determined by extensive spectroscopic analysis and electronic circular dichroism (ECD) spectra. Compounds 1-3 were evaluated for in vitro growth inhibitory activities against four tumor cell lines (MCF-7, NCI-H460, SF-268 and HepG-2), wherein compounds 1 and 3 exhibited considerable growth inhibitory effects, with IC50 values less than 10 μM. [ABSTRACT FROM AUTHOR]

The present study aimed to investigate the variations of the gene network and biological functions induced by hsa‑miR‑145‑5p in the laryngeal squamous cell carcinoma (LSCC) cell line Tu‑177. A hsa‑miR‑145‑5p‑overexpressed Tu‑177 cell model was established, and the gene expression microarray data of miR‑145‑5p‑overexpressed cells and negative control (NC) cells were analyzed. The differentially expressed genes (DEGs) between two groups were identified, and their potential functions were predicted by functional enrichment analysis. Furthermore, the targets of miR‑145‑5p were identified from the DEGs, and their potential functions and protein‑protein interactions (PPIs) were analyzed. The mRNA expressions of acetyl‑CoA carboxylase β (ACACB), fibroblast growth factor receptor 1 (FGFR1), protein phosphatase 3 catalytic subunit a (PPP3CA) and spleen associated tyrosine kinase (SYK), were analyzed via quantitative polymerase chain reaction. A total of 1,501 upregulated and 887 downregulated genes were identified in the hsa‑miR‑145‑5p‑overexpressed Tu‑177 cells, compared with the NC cells. Of these DEGs, 164 upregulated and 221 downregulated genes were predicted to be targeted by hsa‑miR‑145‑5p. The upregulated target genes were primarily associated with functions of immunity, whereas the downregulated target genes were significantly enriched in the p53 signaling pathway. In the PPI network consisting of 267 target genes, the upregulated ACACB had the greatest degree and interacted with downregulated genes including PPP3CA and SYK, in addition to upregulated genes, including FGFR1. The mRNA expressions of ACACB and FGFR1were markedly enhanced in miR‑145‑5p‑overexpressed Tu‑177 cells, whereas overexpressing miR‑145‑5p significantly reduced mRNA expression of PPP3CA and SYK. hsa‑miR‑145‑5p may exhibit an anticancer role in LSCC via regulating multiple cell processes, including cell proliferation and invasion, fatty acid metabolism, immunity and p53 signaling pathway. These findings provide novel information for the future investigation of miR‑145‑5p functions in LSCC. [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs) have emerged recently as important factors in regulating fundamental biological processes. Alterations in the expression and function of lncRNAs have been observed to promote tumor formation, progression and metastasis. Although downregulation of the expression levels of LET lncRNA in several tumors has been reported, its role in gastric cancer remains unknown. The aim of the present study was to investigate the expression and function of LET in gastric cancer development. The expression levels of LET in 37 pairs of gastric cancer and adjacent non-tumor tissues were detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). In addition, LET expression in gastric cancer cell lines was analyzed by RT-qPCR assay analysis. Furthermore, the impact of LET on cell proliferation, migration and apoptosis were detected using the cell counting kit-8, wound scratch and ELISA assays, respectively. The results demonstrated that the expression level of LET was downregulated in gastric cancer tissues and cell lines (SGC-7901 and MGC-803) compared with normal tissues and a normal human gastric epithelial cell line (GES-1). Restoration of LET expression using a synthesized recombinant overexpression vector transfected into SGC-7901 and MGC-803 cells, significantly inhibited cell proliferation and migration, and promoted cell apoptosis in vitro. The present study is the first to demonstrate that LET may function as a tumor suppressor in gastric cancer. The results indicate that LET may be a promising biomarker and/or a therapeutic target for gastric cancer. [ABSTRACT FROM AUTHOR]

Adoptive transfer of cytotoxic T lymphocytes (CTLs) holds promises to cure cancer. However, this treatment is hindered by lacking a robust way to specifically expand out CTLs. Here, we developed a hybrid of B lymphoblastic cell line and T lymphoblastic cell line (T2 cells) as a substitute of dendritic cells, together with irradiated autologous peripheral blood mononuclear cell (PBMC) as feeder cells and rhIL-2, to activate and expand Her-2/neu-specific CD8+ T cells from human epidermal growth factor receptor 2 (Her-2/neu) and human leukocyte antigen (HLA)-A2 double positive advanced breast cancer patients in vitro. These Her-2/neu-loaded T2 cells reproducibly activated and expanded out Her-2/neu-specific CD8+ T cells to 107 in 8 weeks. Furthermore, these Her-2/neu-specific CD8+ T cells had good sensitivity of recognition and killing Her-2/neu-overexpressed breast cancer cell line SK.BR.3. This technique gives us another insight on how to rapidly obtain sufficient CTLs for adoptive cancer immunotherapy. [ABSTRACT FROM AUTHOR]

Rhomboid domain containing 1 (RHBDD1), is a member of the rhomboid protease family, which has a pivotal role in the progression of numerous severe malignancies. However, its role in colorectal carcinoma (CRC) remains to be elucidated. In the present study, RHBDD1 was shown to be widely expressed in CRC cell lines. Lentivirus-mediated RNA interference was employed to knockdown RHBDD1 expression in RKO CRC cells. Functional analyses indicated that depletion of RHBDD1 expression resulted in significantly reduced CRC cell proliferation and colony formation, and induced a G0/G1 phase cell cycle arrest. The findings of the present study suggest that RHBDD1 may contribute to CRC tumorigenesis and serve as a potential therapeutic target in human CRC. [ABSTRACT FROM AUTHOR]