Interleukin (IL)-16, a multifunctional cytokine, plays a fundamental role in inflammatory diseases, as well as in the development and progression of tumors. Genetic variation in the DNA sequence of the IL-16 gene may lead to altered cytokine production and/or activity, and this variation may modulate an individual's susceptibility to both colorectal cancer (CRC) and gastric cancer (GC). To test this hypothesis, we investigated the association of IL-16 gene polymorphisms with serum levels of IL-16 and the risk of CRC and GC in a Chinese population. We analyzed single-nucleotide polymorphisms of the IL-16 gene in 596 cancer patients (376 patients with CRC and 220 patients with GC), and also in 480 age- and sex-matched controls using polymerase chain reaction-restriction fragment length polymorphism and DNA sequencing methods. Serum IL-16 levels were measured by enzyme-linked immunosorbent assay. The rs11556218 T/G polymorphism of the IL-16 gene was significantly associated with the susceptibility to CRC and GC patients. Both male and female patients carrying the G allele had a significantly higher risk for developing CRC and GC compared with individuals carrying the T allele. Alternatively, women carrying the T allele (rs4072111 C/T) showed a decreased risk for CRC and GC compared with individuals carrying the C allele. In patients with CRC or GC, IL-16 serum levels were significantly higher than those in the healthy controls, although no significant association between IL-16 polymorphisms and serum levels of IL-16 was observed. Our data indicate that IL-16 polymorphisms may contribute to CRC and GC susceptibility.

BackgroundA growing body of evidence suggests that microRNAs (miRNAs) play an important role in cancer diagnosis and therapy. MicroRNA-99a (miR-99a), a potential tumor suppressor, is downregulated in several human malignancies. The expression and function of miR-99a, however, have not been investigated in human renal cell carcinoma (RCC) so far. We therefore examined the expression of miR-99a in RCC cell lines and tissues, and assessed the impact of miR-99a on the tumorigenesis of RCC.MethodsMiR-99a levels in 40 pairs of RCC and matched adjacent non-tumor tissues were assessed by real-time quantitative Reverse Transcription PCR (qRT-PCR). The RCC cell lines 786-O and OS-RC-2 were transfected with miR-99a mimics to restore the expression of miR-99a. The effects of miR-99a were then assessed by cell proliferation, cell cycle, transwell, and colony formation assay. A murine xenograft model of RCC was used to confirm the effect of miR-99a on tumorigenicity in vivo. Potential target genes were identified by western blotting and luciferase reporter assay.ResultsWe found that miR-99a was remarkably downregulated in RCC and low expression level of miR-99a was correlated with poor survival of RCC patients. Restoration of miR-99a dramatically suppressed RCC cells growth, clonability, migration and invasion as well as induced G1-phase cell cycle arrest in vitro. Moreover, intratumoral delivery of miR-99a could inhibit tumor growth in murine xenograft models of human RCC. In addition, we also fond that mammalian target of rapamycin (mTOR) was a direct target of miR-99a in RCC cells. Furthermore, siRNA-mediated knockdown of mTOR partially phenocopied the effect of miR-99a overexpression, suggesting that the tumor suppressive role of miR-99a may be mediated primarily through mTOR regulation.ConclusionsCollectively, these results demonstrate for the first time, to our knowledge, that deregulation of miR-99a is involved in the etiology of RCC partially via direct targeting mTOR pathway, which suggests that miR-99a may offer an attractive new target for diagnostic and therapeutic intervention in RCC.

Ultrathin metasurface compromising various sub-wavelength meta-particles offers promising advantages in controlling electromagnetic wave by spatially manipulating the wavefront characteristics across the interface. The recently proposed digital coding metasurface could even simplify the design and optimization procedures due to the digitalization of the meta-particle geometry. However, current attempts to implement the digital metasurface still utilize several structural meta-particles to obtain certain electromagnetic responses, and requiring time-consuming optimization especially in multi-bits coding designs. In this regard, we present herein utilizing geometric phase based single structured meta-particle with various orientations to achieve either 1-bit or multi-bits digital metasurface. Particular electromagnetic wave scattering patterns dependent on the incident polarizations can be tailored by the encoded metasurfaces with regular sequences. On the contrast, polarization insensitive diffusion-like scattering can also been successfully achieved by digital metasurface encoded with randomly distributed coding sequences leading to substantial suppression of backward scattering in a broadband microwave frequency. The proposed digital metasurfaces provide simple designs and reveal new opportunities for controlling electromagnetic wave scattering with or without polarization dependence.

Metasurfaces have promised great possibilities in full control of the electromagnetic wavefront by spatially manipulating the phase characteristics across the interface. Here, we report a scheme to realize broadband backward scattering reduction through diffusion-like microwave reflection by utilizing a flexible indium-tin-oxide (ITO)-based ultrathin coding metasurface (less than 0.1 wavelength thick) with high optical transparence. The diffusion-like scattering is caused by the destructive interference of the scattered far-field electromagnetic wave, which is further attributed to the randomly distributed reflection phases on the metasurface composed of pre-designed meta-atoms arranged with a computer-generated pseudorandom coding sequence. Both simulation and measurement on fabricated prototype sample have been carried out to validate its performance, demonstrating a polarization-independent broadband (nearly from 8 GHz to 15 GHz) 10 dB scattering reduction with good oblique performance. The excellent performances can also be preserved to conformal cases when the flexible metasurface is uniformly wrapped around a metallic cylinder. The proposed metasurface may create new opportunities to tailor the exotic microwave scattering features with simultaneously high transmittance in visible frequencies, which could provide crucial benefits in many practical uses, such as window and solar panel applications.

Several long non-coding RNAs (lncRNAs) have been identified that may have a crucial role in tumor progression and metastasis. The lncRNA cancer susceptibility candidate 2 (CASC2) has previously been reported to act as a tumor suppressor gene in glioma and colorectal cancer. However, the expression and function of CASC2 in renal cell carcinoma (RCC) remains to be elucidated. The present study confirmed that CASC2 was downregulated in human RCC tissues and human RCC cell lines (786‑O and A498). Restoration of CASC2 expression via transfection with a pcDNA3.1(+)‑CASC2 vector was able to inhibit cell proliferation and migration in 786‑O and A498 cells, as compared with in the cells transfected with a pcDNA3.1(+) empty vector. MicroRNA‑21 (miR‑21) has been reported to be upregulated in human RCC tissues and cell lines, and is associated with the malignant progression of RCC. In the present study, bioinformatics analysis and dual‑luciferase reporter assays confirmed that CASC2 was a direct target gene of miR‑21. miR‑21 was able to decrease the expression of CASC2 in 786‑O and A498 cells. Furthermore, overexpression of miR‑21 partly abrogated CASC2‑mediated inhibition of 786‑O and A498 cell proliferation and migration. The present study provides evidence indicating that CASC2 targeted by miR‑21 acts as a tumor suppressor in RCC. Therefore, CASC2 may be considered a novel target for the diagnosis and treatment of RCC.

To study the clinicopathologic characteristics and prognosis of invasive micropapillary carcinoma of breast (IMPC), 100 cases of invasive breast carcinoma with an IMPC component were reviewed. Compared with invasive ductal carcinoma, not otherwise specified, with similar histologic grades, carcinomas with IMPC were larger sized, had a higher lymph node metastasis rate with more nodes involved per case, and exhibited increased lymphovascular invasion. The presence of IMPC strongly correlated with the more aggressive behavior. No significant association was established between the proportion of the IMPC component and overall tumor size, histologic grade, lymph node metastasis rate, and distant metastasis, but a trend was noted. Long-term follow-up demonstrated a poorer 5-year and 10-year survival rate for patients with breast carcinoma containing an IMPC component. Breast carcinomas with micropapillary features are more aggressive tumors with a poorer prognosis. This specific structure should be carefully evaluated in the surgical pathology examination of breast carcinoma specimens.

All these tests indicated that cycloxaprid had both contact and root-systemic activity, with sublethal effects resulting in reduction in Sitobion avenae phloem-feeding behaviour and growth rate.

Epigallocatechin gallate (EGCG), the major biologically active compound in green tea, is a well-known chemoprevention agent. Although several reports have shown that EGCG exerts its anticancer activity by targeting specific cell signaling pathways, the underlying molecular mechanism(s) are only partially understood. In the present study, we report that EGCG had a profound antiproliferative effect on human lung cancer cells. EGCG inhibited anchorage-independent growth and induced cell cycle G0/G1 phase arrest. The mechanism underlying EGCG antitumor potency was mainly dependent on suppression of the EGFR signaling pathway. Short-term EGCG exposure substantially decreased EGF-induced EGFR, AKT and ERK1/2 activation. Moreover, long-term EGCG treatment not only inhibited total and membranous EGFR expression, but also markedly attenuated EGFR nuclear localization and expression of the downstream target gene cyclin D1, indicating that EGCG treatment suppressed EGFR transactivation. Additionally, knockdown of EGFR in lung cancer cells decreased their sensitivity to EGCG. Thus, inhibition of the EGFR signaling pathway may partly contribute to the anticancer activity of EGCG.