MicroRNAs (miRNAs) are highly conserved noncoding RNAs of about 19-25 nucleotides. Through specifically pairing with complementary sites in 3' untranslated regions (UTRs) of target mRNAs, they mediate post-transcriptional silencing. MicroRNAs have been implicated in many physiological processes including proliferation, differentiation, development, apoptosis, and metabolism. In recent years many studies have revealed that the aberrant expression of miRNA is closely related to oncogenesis and is now an intense field of study. Mir-148a is aberrantly expressed in various cancers and has been identified as an oncogenic or tumor suppressor with crucial roles in the molecular mechanisms of oncogenesis. In this review, we have summarized the role of mir-148a in the oncogenic pathways of gastric, liver, breast and urogenital cancers, and in neurogliocytoma oncogenesis. Studying the functional role of mir-148a is crucial in discovering novel tumor molecular markers and identifying potential therapeutic targets.

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The rising atmospheric CO2 concentration (Ca) has increased tree growth and intrinsic water-use efficiency (iWUE). However, the magnitude of this effect on long-term iWUE and whether this increase could stimulate the growth of riparian forests in extremely arid regions remain poorly understood. We investigated the relationship between growth [ring width; basal area increment (BAI)] and iWUE in a riparian Populus euphratica Oliv. forest to test whether growth was enhanced by increasing CO2 and whether this compensated for environmental stresses in the lower reaches of the inland Heihe River, northwestern China. We accomplished this using dendrochronological methods and carbon (δ(13)C) and oxygen (δ(18)O) isotopic analysis. We found an increase in BAI before 1958, followed by a decrease from 1958 to 1977 and an increase to a peak around 2000. Tree-ring carbon discrimination (Δ) and δ(18)O indicated significant negative overall trends from 1920 to 2012. However, the relationship shifted in strength and direction around 1977 from significantly negative to a weak connection. The seasonal minimum temperature in April to July showed strong influence on Δ, and δ(18)O was controlled by relative humidity (negatively correlated) and temperature (positively correlated) in June and July. The patterns of internal to atmospheric CO2 (Ci/Ca) suggest a specific adaptation of tree physiology to increasing CO2. Intrinsic water-use efficiency increased significantly (by 36.4%) during the study period. The increased iWUE explained 19.8 and 39.1% of the observed yearly and high-frequency (first-order difference) variations in BAI, respectively, after 1977. Our results suggest significant CO2 stimulation of riparian tree growth, which compensated for the negative influences of reductions in river streamflow and a drying climate during the study period.

Rising atmospheric CO2 concentration (Ca) is expected to accelerate tree growth by enhancing photosynthesis and increasing intrinsic water-use efficiency (iWUE). However, the extent of this effect on long-term iWUE and its interactions with climate remains unclear in trees along an elevation gradient. Therefore, we investigated the variation in the radial growth and iWUE of mature Picea schrenkiana trees located in the upper tree-line (A1: 2700 m a.s.l.), middle elevation (A2: 2400 m a.s.l.), and lower forest limit (A3: 2200 m a.s.l.), in relation to the rising Ca and changing climate in the Wusun Mountains of northwestern China, based on the basal area increment (BAI) and tree-ring δ13C chronologies from 1960 to 2010. We used the CRU TS3.22 dataset to analyze the general response of tree growth to interannual variability of regional climate, and found that BAI and δ13C are less sensitive to climate at A1 than at A2 and A3. The temporal trends of iWUE were calculated under three theoretical scenarios, as a baseline for interpreting the observed gas exchange at increasing Ca. We found that iWUE increased by 12–32% from A1 to A3 over the last 50 years, and showed an elevation-dependent variation in physiological response. The significant negative relationship between BAI and iWUE at A2 and A3 showed that tree growth has been decreasing despite long-term increases in iWUE. However, BAI remained largely stable throughout the study period despite the strongest iWUE increase [at constant intercellular CO2 concentration (Ci) before 1980] at A1. Our results indicate a drought-induced limitation of tree growth response to rising CO2 at lower elevations, and no apparent change in tree growth and diminished iWUE improvement since 1980 in the upper tree-line. This study may contradict the expectation that combined effects of elevated Ca and rising temperatures have increased forest productivity, especially in high-elevation forests.

Previous studies have identified several HLA-B specificities that are associated with nasopharyngeal carcinoma (NPC) in populations of Chinese descent, in particular HLA-B35, -B38, -B46, and -B58. Perhaps except for HLA-B46, other associations cannot be simply accounted for by the linkage disequilibrium between HLA-A and B loci. The human major histocompatibility complex (MHC) class I chain-related gene A (MICA) maps 46 kb centromeric to HLA-B and is highly polymorphic; it encodes a stress-inducible protein which functions as a ligand for the NKG2D/DAP10 complex to activate natural killer (NK) cells, gammadelta T cells, and CD8(+) T cells. We postulated MICA gene as a susceptibility factor for nasopharyngeal carcinoma, an Epstein-Barr virus-associated malignancy. In this study, 218 unrelated patients newly diagnosed with NPC and 196 randomly selected healthy controls from southern China mainland were analyzed for the short tandem repeat polymorphism of exon 5 of MICA gene (MICA-STR) and MICA gene deletion, using fluorescent polymerase chain reaction-gene scanning (PCR/size-sequencing) and polymerase chain reaction-sequence-specific priming (PCR/SSP) technology. MICA*A9 was present at significantly increased frequency in the patient group (P (C)=0.0001002, OR=2.528, 95% CI=1.636-3.907), whereas the frequency of MICA*A5.1 was significantly decreased (P (C)=0.006, OR=0.594, 95% CI=0.437-0.806). Gender-based stratification revealed a significant increase of MICA*A9 frequency (P (C)=0.000072, OR=3.255, 95% CI=1.855-5.709) and a significant decrease of MICA*A5.1 frequency (P (C)=0.000737, OR=0.486, 95% CI=0.337-0.702) in male patients with NPC (N=166), compared with male normal controls (N=120). A significant interaction between MICA*A9 and gender was observed ([see text]=41.58, P=0.0001). Statistics also revealed heterogeneity of effects among MICA*A5.1/MICA*A9-bearing phenotypes and a dose-dependent effect of MICA*A5.1 and MICA*A9 on NPC risk in male subgroup. This constitutes the first demonstration of a gender-specific association between MICA-STR polymorphism and NPC, which could largely be attributable to the underlying gender-related mechanisms that modulate MICA gene expression. The results provide strong supporting evidence suggesting that MICA*A9 may be a genetic risk factor for NPC in male individuals in this population. The potential interaction between MICA and other non-HLA host factors and environmental exposures remains to be further studied.

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BackgroundAn association between male subfertility and an increased risk of testicular cancer has been proposed, but conflicting results of research on this topic have rendered this theory equivocal. To more precisely assess the association between subfertility and the risk of testicular cancer, we performed a systematic review of international epidemiologic evidence.Principal FindingsWe searched the Medline database for records from January 1966 to March 2008 complemented with manual searches of the literature and then identified studies that met our inclusion criteria. Study design, sample size, exposure to subfertility and risk estimates of testicular cancer incidence were abstracted. Summary relative risks (RRs) with 95% confidence intervals (CIs) were calculated using the DerSimonian and Laird model. All statistical tests were two-sided. We identified seven case-control studies and two cohort studies published between 1987 and 2005. Analysis of the seven case-control studies that included 4,954 participants revealed an overall statistically significant association between subfertility and increased risk of testicular cancer (summary RR = 1.68, 95% CI: 1.22 to 2.31), without heterogeneity between studies (Q = 8.46, P heterogeneity = 0.21, I 2 statistics = 0.29). The association between subfertility and testicular cancer was somewhat stronger in the United States (summary RR = 1.75, 95% CI: 1.01 to 3.02) than it was in Europe (summary RR = 1.53, 95% CI: 1.22 to 1.92). The source of the control subjects had a statistically significant effect on the magnitude of the association (population-based summary—RR = 2.15, 95% CI: 1.11 to 4.17; hospital-based summary—RR = 1.56, 95% CI: 0.93 to 2.61). After excluding possible cryptorchidism, an important confounding factor, we also found a positive association between subfertility and increased risk of testicular cancer (summary RR = 1.59, 95% CI: 1.28 to 1.98). These results were consistent between studies conducted in the United States and in Europe (Q = 0.20, P heterogeneity = 0.66). Of the two cohort studies that reported standardized incidence ratios, both reported a statistically significant positive association between subfertility and increased risk of testicular cancer.ConclusionsOur findings support a relationship between subfertility and increased risk of testicular cancer and apply to the management of men with subfertility, and prevention and diagnosis of testicular cancer.