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[This retracts the article DOI: 10.1016/j.omtn.2020.10.035.].
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Diverse higher-order structures, foundational for supporting a network's "meta-functions", play a vital role in structure, functionality, and the emergence of complex dynamics. Nevertheless, the problem of dismantling them has been consistently overlooked. In this paper, we introduce the concept of dismantling higher-order structures, with the objective of disrupting not only network connectivity but also eradicating all higher-order structures in each branch, thereby ensuring thorough functional paralysis. Given the diversity and unknown specifics of higher-order structures, identifying and targeting them individually is not practical or even feasible. Fortunately, their close association with k-cores arises from their internal high connectivity. Thus, we transform higher-order structure measurement into measurements on k-cores with corresponding orders. Furthermore, we propose the Belief Propagation-guided Higher-order Dismantling (BPHD) algorithm, minimizing dismantling costs while achieving maximal disruption to connectivity and higher-order structures, ultimately converting the network into a forest. BPHD exhibits the explosive vulnerability of network higher-order structures, counterintuitively showcasing decreasing dismantling costs with increasing structural complexity. Our findings offer a novel approach for dismantling malignant networks, emphasizing the substantial challenges inherent in safeguarding against such malicious attacks.
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Circular RNAs (circRNAs) are a class of non-coding RNAs broadly expressed in cells of various species. However, the contributions and molecular mechanisms of circRNAs to hepatocellular carcinoma (HCC) remain largely unknown. In the present study, we compared the expression of circRNAs between five paired HCC and adjacent noncancerous liver (ANL) tissues by using RNA-sequencing (RNA-seq). circRASGRF2 (a circRNA located on chromosome 5 and derived from RASGRF2, hsa_circ_0073181) was identified and validated by quantitative reverse transcriptase PCR. The role of circRASGRF2 in HCC progression was assessed both in vitro and in vivo. Mechanistically, RNA immunoprecipitation and luciferase reporter assays were performed to confirm the interaction between circRASGRF2 and miR-1224 in HCC. circRASGRF2 was found to be significantly upregulated in HCC tissues and HCC cell lines compared with paired ANL tissues and normal cells. Our in vivo and in vitro data indicated that knockdown of circRASGRF2 inhibits the proliferation and migration of HCC cells. Mechanistically, we found that circRASGRF2 could promote the expression of focal adhesion kinase (FAK) by sponging miR-1224. Our data showed that circRASGRF2 is a central component linking circRNAs to progression of HCC, making it a potential therapeutic target.
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Long non-coding RNAs (lncRNAs) play essential roles in diverse biological processes; however, current understanding of the mechanism underlying the regulation of tumour proliferation and metastasis is limited. Lung cancer-associated transcript 1 (LUCAT1) has been reported in a variety of human cancers, while its role in hepatocellular carcinoma (HCC) remains unclear. This study aimed to determine the biological role and underlying mechanism of LUCAT1 on progression and metastasis in HCC cells and clinical specimens. Our results demonstrated that LUCAT1 was up-regulated in HCC tissues and cells. Loss- and gain-of-function studies revealed that LUCAT1 promotes the proliferation and metastasis of HCC cells in vitro and in vivo. Furthermore, RNA pulldown and Western blot assays indicated that LUCAT1 inhibited the phosphorylation of Annexin A2 (ANXA2) to reduce the degradation of ANXA2-S100A10 heterotetramer (AIIt), which in turn accelerated the secretion of plasminogen into plasmin, thereby resulting in the activation of metalloprotease proteins. In conclusion, we propose that LUCAT1 serves as a novel diagnostic and therapeutic target for HCC.