Background: The expression of circRNA_100269 in gastric cancer (GC) tissues and cells, together with its regulatory roles on GC cells were investigated. Methods: The levels of circRNA_100269 in GC and matched para-carcinoma tissues, as well as in human GC cell lines and normal gastric epithelial cells were evaluated using RT-qPCR. The models with overexpression or knockdown of circRNA_100269 were generated using lentiviral vectors. Cell viability was examined using MTT assay; cell migration and invasive activity were determined by wound healing and Transwell assay. Cell cycle arrest and apoptosis were assessed; molecules involved in PI3K/Akt signaling, apoptosis and EMT were evaluated using RT-qPCR and immunoblotting. Tumour growth and expression of relevant proteins were examined in circRNA_100269 knockout mice.Results: The results indicated the expression of circRNA_100269 was dramatically decreased in GC samples compared with para-carcinoma tissues (p<0.05), while the levels of PI3K were notably increased (p<0.05). Moreover, the level of circRNA_100269 was relevant to histology grade and occurrence of metastasis in GC patients (p<0.05), where circRNA_100269 and PI3K was inversely correlated (p<0.05). Additionally, circRNA_100269 was downregulated in GC cells compared with normal gastric epithelial cells. Overexpressed circRNA_100269 remarkably suppressed the proliferation, migration, invasion and EMT of GC cells (p<0.05), induced cell cycle arrest at G0/G1 phase and promoted cell apoptosis (p<0.05). In addition, PI3K/Akt signaling was involved in circRNA_100269-mediated proliferation, migration, invasion, EMT and apoptosis in GC cells (p<0.05). Knockdown of circRNA_100269 also significantly promoted tumor growth in vivo (p<0.05). Conclusions: the data of the present study suggested that the expression level of circRNA_100269 was decreased in GC tissues and cells. In addition, circRNA_100269 inhibited the progression of GC by suppressing PI3K/Akt signaling. Therefore, circRNA_100269/PI3K/Akt axis may be a potential therapeutic target for GC treatment.
Metasurfaces have intrigued long-standing research interests and developed multitudinous compelling applications owing to their unprecedented capability for manipulating electromagnetic waves, and the emerging programmable coding metasurfaces (PCMs) provide a real-time reconfigurable platform to dynamically implement customized functions. Nevertheless, most existing PCMs can only act on the single polarization state or perform in the limited polarization channel, which immensely restricts their practical application in multitask intelligent metadevices. Herein, an appealing strategy of the PCM is proposed to realize tunable functions in co-polarized reflection channels of orthogonal circularly polarized waves and in co-polarized and cross-polarized reflection channels of orthogonal linearly polarized waves from 9.0 to 10.5 GHz. In the above six channels, the spin-decoupled programmable meta-atom can achieve high-efficiency reflection and 1-bit digital phase modulation by selecting the specific ON/OFF states of two diodes, and the phase coding sequence of the PCM is dynamically regulated by the field-programmable gate array to generate the desired function. A proof-of-concept prototype is constructed to verify the feasibility of our methodology, and numerous simulation and experimental results are in excellent agreement with the theoretical predictions. This inspiring design opens a new avenue for constructing intelligent metasurfaces with higher serviceability and flexibility, and has tremendous application potential in communication, sensing, and other multifunctional smart metadevices.
Background: The expression of circRNA_100269 in gastric cancer (GC) tissues and cells, together with its regulatory roles on GC cells were investigated. Methods: The levels of circRNA_100269 in GC and matched para-carcinoma tissues, as well as in human GC cell lines and normal gastric epithelial cells were evaluated using RT-qPCR. The models with overexpression or knockdown of circRNA_100269 were generated using lentiviral vectors. Cell viability was examined using MTT assay; cell migration and invasive activity were determined by wound healing and Transwell assay. Cell cycle arrest and apoptosis were assessed; molecules involved in PI3K/Akt signaling, apoptosis and EMT were evaluated using RT-qPCR and immunoblotting. Tumour growth and expression of relevant proteins were examined in circRNA_100269 knockout mice. Results: The results indicated the expression of circRNA_100269 was dramatically decreased in GC samples compared with para-carcinoma tissues (p < 0.05), while the levels of PI3K were notably increased (p < 0.05). Moreover, the level of circRNA_100269 was relevant to histology grade and occurrence of metastasis in GC patients (p < 0.05), where circRNA_100269 and PI3K was inversely correlated (p < 0.05). Additionally, circRNA_100269 was downregulated in GC cells compared with normal gastric epithelial cells. Overexpressed circRNA_100269 remarkably suppressed the proliferation, migration, invasion and EMT of GC cells (p < 0.05), induced cell cycle arrest at G0/G1 phase and promoted cell apoptosis (p < 0.05). In addition, PI3K/Akt signaling was involved in circRNA_100269-mediated proliferation, migration, invasion, EMT and apoptosis in GC cells (p < 0.05). Knockdown of circRNA_100269 also significantly promoted tumor growth in vivo (p < 0.05). Conclusions: the data of the present study suggested that the expression level of circRNA_100269 was decreased in GC tissues and cells. In addition, circRNA_100269 inhibited the progression of GC by suppressing PI3K/Akt signaling. Therefore, circRNA_100269/PI3K/Akt axis may be a potential therapeutic target for GC treatment.
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