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Non-orthogonal multiple access (NOMA) is a promising emerging technology that can significantly improve the utilization of spectrum and system capacity in heterogeneous wireless networks. Power allocation plays a key role in the successful deployment of NOMA. In the most prior power allocation schemes, the perfect channel state information (CSI) is assumed to be known which is difficult to obtain in a realistic environment. In this paper, we propose a power allocation scheme to maximize energy efficiency of small cells for downlink NOMA heterogeneous networks based on imperfect CSI. The system model for imperfect CSI is built, in which the optimization problem is a probabilistic non-convex problem with the constraint of outage probability. To solve the optimization problem, the probabilistic problem is transformed to a non-probabilistic problem through relaxation. The power allocation for each small cell is achieved via bisection search algorithm based on gradient value, where the trend of energy efficiency as a function of the power of the small cell is analyzed. The sequential convex programming is adapted to transform the non-convex problem to a convex problem. The closed-form solutions of power allocation factors are derived by the Lagrangian multiplier method. The simulation results show the superiority and efficiency of the proposed scheme compared with the traditional algorithms.INDEX TERMS Heterogeneous networks, non-orthogonal multiple access, power allocation, imperfect channel state information, energy efficiency.

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Introduction Lung cancer (LC) is among the most prevalent malignancies worldwide, with extremely high morbidity and mortality rates. Mounting evidence has suggested that the abnormally expressed long noncoding RNA (lncRNA) in lung cancer tissues may play vital roles in tumor progression. In the present research, we aimed to examine the functions and underlying mechanism of linc01833 in lung adenocarcinoma (LUAD). Methods qRT-PCR was employed to determine transfection efficiency. CCK-8, transwell invasion assay, Western blotting analysis and qRT-PCR were used to detect proliferation as well as migration of different LUAD cell lines, and were also applied to determine the changes during epithelial–mesenchymal transformation (EMT). Afterwards, bioinformatics and dual-luciferase reporter assay were utilized to explore and to identify the potential corresponding targets of linc01833 and miR-519e-3p. Results Linc01833 OE can significantly improve proliferation as well as invasion ability of LC cells and promote the EMT process. Dual-luciferase reporter assay demonstrated that linc01833 could directly bind to miR-519e-3p, thereby inhibiting its expression. Further experiments showed that S100A4 was a direct target of miR-519e-3p. Rescue assay demonstrated that linc01833 acted on the miR-519e-3p/S100A4 axis. Conclusion We verified the mechanism of linc01833 in promoting infiltration and metastasis in LUAD. To be specific, linc01833 can function as a competitive endogenous RNA (ceRNA) to adsorb miR-519e-3p through a sponge and regulate S100A4 in lung cancer, thereby being involved in LUAD progression. Collectively, our research provides new insights towards the in-depth understanding of LC progression mechanisms.

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