Colorectal cancer (CRC) is the third most common cancer type and the fourth leading cause of cancer‑associated mortality worldwide. MicroRNA (miR)‑1246 is involved in differentiation, invasion, metastasis and chemoresistance of certain types of tumor cells. CCNG2 encodes an unconventional cyclin homolog, cyclin G2 (CycG2), associated with growth inhibition, which correlated significantly with lymph node metastasis, clinical stage, histological grade and poor overall survival in numerous cancer types. To investigate the regulation of miR‑1246 on CycG2 expression, and their effects on proliferation and metastasis of CRC, HCT‑116 and LOVO cells were transfected with pre‑miR‑1246 anti‑miR‑1246 and their negative controls. It was demonstrated that the expression of miR‑1246 was significantly increased in CRC tissues and cell lines, which was the opposite of CycG2. miR‑1246 negatively regulated the expression of CycG2 in HCT‑116 and LOVO CRC cells. CCNG2 is a direct target of miR‑1246 in CRC cells. Overexpression of miR‑1246 induced cell proliferation, migration and invasion, while knockdown of miR‑1246 inhibited proliferation, migration and invasion in the CRC cells. Upregulation of miR‑1246 mediated the malignant progression of CRC and is partly attributed to the downregulation of the expression of CycG2. Consequently, these findings provided a molecular basis for the role of miR‑1246/CCNG2 in the progression of human CRC and suggested a novel target for the treatment of CRC.

1. TCs can accelerate the migration of MSCs from the intraperitoneal space into injured lung tissues through intercellular signals and/or cell-cell interaction. 2. Pre-activated MSCs and TCs with LPS show more efficient in cell-cell communication by OPN-or EGFR-dominated signal pathways

Quantification of soil structure is important for understanding soil behavior. The objectives of this study were to: (i) introduce the use of the point‐distribution method (PDM) for calculating fractal parameters of soil density (ρb), and (ii) introduce the use of fractal lacunarity in conjunction with the fractal dimension for quantifying small‐scale soil structure data collected with x‐ray computed tomography. Undisturbed silt loam soil cores were taken from forest and grassland sites. Additional silt loam soil collected from a nearby cultivated field was sieved and repacked in 76‐mm‐diam. cores. Four cores were packed with soil passing through a 2‐mm sieve but retained on a 1‐mm sieve (1–2 mm). Four additional cores were packed with the soil passing through a 1‐mm sieve (<1 mm). Computed tomography (CT) was used to measure small‐scale ρb of each 0.1 by 0.1 by 2 mm volume element (voxel) of a slice through a soil core. Calculation of fractal dimension and lacunarity was accomplished using the PDM on CT ρb data. Results show that CT ρb data are fractal when analyzed using the PDM. Mean fractal dimension (±SD) of the forest, grassland, <1 mm, and 1‐ to 2‐mm groups were 2.42 ± 0.13, 2.35 ± 0.14, 2.50 ± 0.025, and 2.47 ± 0.013, respectively. Corresponding mean fractal lacunarity of these four groups at a voxel size of 3.1 mm were 0.24 ± 0.025, 0.24 ± 0.019, 0.16 ± 0.005, and 0.20 ± 0.012. Fractal lacunarity, which reflects the second‐order statistics of ρb, or the uniformity of pores and aggregates within a soil core, is essential for discriminating soils of similar but slightly different structure.

Background Obstructive sleep apnea (OSA) is associated with cancer incidence and mortality. The underlying mechanism is unclear. This study aims to evaluate the influence of intermittent hypoxia (IH), a novel hallmark of OSA, on tumor and to access the anti-tumor effect of endostatin on a mouse model with OSA. Methods The C57BL/6 J mice were randomly classified into four groups: control (normoxia) (CTL), control plus endostatin (CTL + ED), IH, and IH plus endostatin (IH + ED). Mice in IH and IH + ED groups were subjected to IH 8 h per day in 5 weeks. Lewis lung cancer cells were injected into the flank of each mouse after 1 week of IH exposure. Endostatin was also intraperitoneally injected after tumor volume reached about 200 mm 3. The maximum standard uptake values (SUVmax) were detected by micro-positron emission tomography-computed tomography (micro-PET-CT) imaging prior and postendostatin administration. Microvessel density (MVD) and vascular endothelial growth factor (VEGF) were determined for evaluating the anti-tumor effect of endostatin among the normoxia and IH conditions. Results Mice had higher SUVmax in the IH group than the CTL group (p < 0.01). When compared with mice in the CTL group, those in the IH group had significantly greater MVD values (p < 0.001). The SUVmax can be attenuated by endostatin both in the CTL (p < 0.01) and IH conditions (p < 0.001). When compared with CTL group, mice in the IH group had increased MVD values (p < 0.001) and VEGF expression both at mRNA (p < 0.05) and protein levels (p < 0.001 in western blotting results). Treatment with endostatin attenuated serum and tissue VEGF levels, lowering the MVD values. As compared to normoxia condition, the endostatin-therapeutic effects were more significant under the IH condition (p < 0.05 in western blotting results). Conclusions Micro-PET-CT imaging is a promising non-invasive technique to evaluate the tumor metabolic characteristics under IH condition in vivo. The anti-tumor effect of endostatin under IH condition is superior to that of the normoxia condition.

Background: As a hallmark of obstructive sleep apnea (OSA), intermittent hypoxia (IH) promotes tumor progress. The high expression of programmed death 1 and programmed death ligand 1 (PD-L1) in tumor leads to immune evasion and subsequently aggravates tumor progress. This study aims to determine the tumor PD-L1 expression under the IH condition.Methods: A total of 24 C57BL/6J mice were randomly assigned to the normoxia (control, CTL) group and the IH group. Mice in the IH group were subjected to the IH condition for 5 weeks. Lung cancer cells were injected into the flank of each mouse after 1 week of IH exposure. Tumor PD-L1 expression was detected by immunohistochemistry (IHC). Correlation between tumor weight, tumor volume, and expression of PD-L1 was analyzed.Results: Compared to the CTL group, mice in the IH group had a high PD-L1 expression. The IH can enhance the tumor PD-L1 expression. Tumor weight, volume, and HIF-1α levels were closely associated with the PD-L1 expression in the IH group, while dissimilar findings were observed in the CTL group. Conclusions:The IH enhances tumor PD-L1 expression in OSA mimicking mice. Additional studies are required to clarify the underlying mechanism.