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Benzo[a]pyrene (BaP), a representative polycyclic aromatic hydrocarbon compound, is a carcinogen that causes head and neck cancers. Despite intensive research, the molecular mechanism of BaP in the development of oral squamous cell carcinoma (OSCC) remains largely unknown. In the present study, the SCC‐9 human OSCC cell line was cultured in vitro, separated into treatment groups, and treated with dimethyl sulfoxide or BaP at various concentrations. The malignant behavior ascribed to the BaP treatment was investigated by cell proliferation, clony formation assay, and Transwell assays. Furthermore, transcriptome sequencing was performed to detect the differentially expressed genes, followed by quantitative real‐time PCR to measure the expression levels of nine of these genes. Moreover, the Gene Ontology (GO) term and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses showed the biological processes and signaling pathways in which the target genes were involved. Significant effects on SCC‐9 cell proliferation, tumorigenicity, cell migration, and invasion were observed after exposure to 8 μM BaP. Additional results revealed that BaP inhibited apoptosis in a dose‐dependent manner. The transcriptome sequencing results showed 137 upregulated genes and 135 downregulated genes induced by BaP, associated with tumor‐related biological processes and signaling pathways, mainly including transcriptional dysregulation in cancer, the tumor necrosis factor signaling pathway, metabolism of xenobiotics by cytochrome P450, mitogen‐activated protein kinase signaling pathway, and so forth. Our study demonstrates that BaP may regulate the expression of certain genes involved in tumor‐associated signaling pathways, thereby promoting the proliferative, tumorigenic, and metastatic behaviors of OSCC cells while suppressing their apoptosis. [ABSTRACT FROM AUTHOR]

Aims: Understanding the joint effects of plant development and environment on shifts of intraspecific leaf traits will advance the understandings of the causes of intraspecific trait variation. We address this question by focusing on a widespread species Clausena dunniana in a subtropical broad‐leaved forest. Methods: We sampled 262 individuals of C. dunniana at two major topographic habitat types, the slope and hilltop, within the karst forests in Maolan Nature Reserve in southwestern China. We measured individual plant level leaf traits (i.e., specific leaf area (SLA), leaf area, leaf dry‐matter content (LDMC), and leaf thickness) that are associated with plant resource‐use strategies. We adopted a linear mixed‐effects model in which the plant size (i.e., the first principal component of plant basal diameter and plant height) and environmental factors (i.e., topographic habitat, canopy height, and rock‐bareness) were used as independent variables, to estimate their influences on the shifts of leaf traits. Key Results: We found that (1) plant size and the environmental factors independently drove the intraspecific leaf trait shifts of C. dunniana, of which plant size explained less variances than environmental factors. (2) With increasing plant size, C. dunniana individuals had increasingly smaller SLA but larger sized leaves. (3) The most influential environmental factor was topographic habitat; it drove the shifts of all the four traits examined. Clausena dunniana individuals on hilltops had leaf traits representing more conservative resource‐use strategies (e.g., smaller SLA, higher LDMC) than individuals on slopes. On top of that, local‐scale environmental factors further modified leaf trait shifts. Conclusions: Plant size and environment independently shaped the variations in intraspecific leaf traits of C. dunniana in the subtropical karst forest of Maolan. Compared with plant size, the environment played a more critical role in shaping intraspecific leaf trait variations, and potentially also the underlying individual‐level plant resource‐use strategies. [ABSTRACT FROM AUTHOR]

Aim: To evaluate the role of radiotherapy (RT) in the treatment of localized primary adult rhabdomyosarcoma (RMS). Methods: This retrospective study identified 62 consecutive adult patients with localized primary RMS from January 2000 and July 2016. Local failure‐free survival (LFFS), distant metastasis‐free survival (DMFS) and overall survival (OS) were analyzed by the Kaplan–Meier method. Multivariate Cox proportional hazards regression models were fit to assess the ability of patient characteristics to predict survival. Results: With a median follow‐up of 33 months (range, 6–195 months), the 5‐year LFFS, DMFS and OS of all patients were 64.0%, 50.0% and 45.0%, respectively. RT was administered to 28 patients (45.2%). Patients who received RT had a higher 5‐year LFFS (81.7% vs 47.2%), 5‐year DMFS (59.4% vs 43.1%) and 5‐year OS (57.1% vs 34.8%) compared with patients who did not received RT. In mulitvariate analysis, RT retained significance as an independent predictor of improved LFFS [hazard ratio (HR) = 0.282; 95% confidence interval (CI), 0.095–0.838; P = 0.023], DMFS (HR = 0.289; 95% CI, 0.125–0.991; P = 0.004) and OS (HR = 0.334; 95% CI, 0.153–0.727; P = 0.006). Conclusions: RT significantly reduced local recurrence, distant metastasis and tumor mortality compared with no radiotherapy for localized primary adult RMS. [ABSTRACT FROM AUTHOR]

Despite the recent development of treatment strategies for nasopharyngeal carcinoma, the effective management of this disease remains a challenging clinical problem. A better understanding of the regulatory roles of miR‐194 and mitogen‐activated protein kinase kinase kinase 3 (MAP3K3) in the nasopharyngeal‐carcinoma‐related gene network is required to address this issue. Here, we measured relative expression of miR‐194 in human nasopharyngeal carcinoma tissues and normal epithelial tissues by quantitative real time PCR. We transfected cultured CNE‐1 and C666‐1 cells with miR‐194 mimics, and then examined the effects on cell proliferation, cell migration and invasion. Luciferase reporter assay was used to validate the putative binding between miR‐194 and MAP3K3. We then examined the effect of knockdown and overexpression of MAP3K3 on cell tumorigenesis. Expression of miR‐194 is significantly down‐regulated in nasopharyngeal carcinoma specimens and tumor cell lines when compared with normal controls. In addition, miR‐194 suppressed tumor cell proliferation and viability, as well as migration and invasion of carcinoma cells. We found that miR‐194 binds the 3′ untranslated region of MAP3K3, and knockdown of miR‐194 inhibited nasopharyngeal carcinoma cell proliferation, migration and invasion. In accordance, overexpression of MAP3K3 reversed the inhibitory effects of miR‐194 in carcinoma cells. This study suggests that expression of miR‐194 is down‐regulated in nasopharyngeal carcinoma, and that miR‐194 can directly target MAP3K3 to regulate tumor progression. Given the pivotal involvement of MAP3K3 in nasopharyngeal carcinoma development, targeting miR‐194 may be a novel strategy for the treatment of nasopharyngeal carcinoma. miR‐194 was down‐regulated in nasopharyngeal carcinoma. miR‐194 can directly target MAP3K3 for regulating tumor progression. Given the pivotal involvement of MAP3K3 in nasopharyngeal carcinoma development, targeting miR‐194 could provide a novel strategy for the treatment of nasopharyngeal carcinoma. [ABSTRACT FROM AUTHOR]