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The role of circRNAs in esophageal squamous cell cancer (ESCC) remains unclear. Here we profiled six pair plasma circRNA in ESCC based on RNA sequencing, and then verified the elevation of hsa_circ_0004771 in 20 cancer tissues and 105 pair case–control plasma samples by quantitative reverse transcriptase PCR. The upregulation of hsa_circ_0004771 was correlated with heavier tumor burden and poor prognosis, knockdown of it inhibited the ESCC cells proliferation both and . Mechanistically, hsa_circ_0004771 positively regulated CDC25A by acting as a molecular sponge of miR-339-5p and rescue assay confirmed this regulatory relationship. These results suggested that hsa_circ_0004771 can serve as a general less-invasive biomarker and may provide diagnostic and prognostic value in carcinoma.

Using the framework of an investigation of the stimuli-responsive behavior of peptide assembly on a solid surface, this study on the behavior of a chemisorbed peptide on a gold surface was performed. The studied peptide is a dimeric form of the antimicrobial peptide Trichogin GAIV, which was also modified by substituting the glycine with lysine residues, while the N-terminus octanoyl group was replaced by a lipoic one that was able to bind to the gold surface. In this way, a chemically linked peptide assembly that is pH-responsive was obtained because of the protonation/deprotonation of the sidechains of the Lys residues. Information about the effect of protonation/deprotonation equilibria switching the pH from acid (pH = 3) to basic (pH = 11) conditions was obtained macroscopically by performing Quartz crystal microbalance with dissipation monitoring (QCM-D), Surface Plasmon Resonance (SPR), Nanoplasmonic Sensing (NPS), and FTIR techniques. Using molecular dynamics (MD) simulations, it is possible to explain, at the molecular level, our main experimental results: (1) pH changes induce a squeezing behavior in the system, consisting in thickness and mass variations in the peptide layer, which are mainly due to the pH-driven hydrophilic/hydrophobic character of the lysine residues, and (2) the observed hysteresis is due to small conformational rearrangements from helix to beta sheets occurring mainly on the first half of the peptide, closer to the surface, while the second half remains almost unaffected. The latter result, together with the evidence that the layer thickness is not simply double the assembly of the monomeric analog, indicates that the dimeric peptide does not behave as a double monomer, but assumes very peculiar features.

As previously reported, long intergenic non-protein-coding RNA 1006 (LINC01006) plays crucial roles in prostate, pancreatic and gastric cancers. However, whether it plays important roles in cervical cancer remains unclear. The present study thus aimed to determine the precise role of LINC01006 in cervical cancer and elucidate its regulatory mechanisms. The expression of LINC01006 in cervical cancer was examined by reverse transcription-quantitative polymerase chain reaction. Cell proliferation assay, flow cytometric analysis, Transwell migration and invasion assays, and tumor xenograft model experiments were performed to elucidate the roles of LINC01006 in cervical cancer. Bioinformatics analysis, luciferase reporter assay, RNA immunoprecipitation and rescue experiments were performed for mechanistic analyses. The expression of LINC01006 was found to be upregulated in cervical cancer and to be associated with a poor prognosis. The absence of LINC01006 inhibited the proliferation, migration and invasion of cervical cancer cells, whereas it promoted cell apoptosis in vitro. The downregulation of LINC01006 impeded tumor growth in vivo. LINC01006 was verified as an endogenous 'sponge' that competed for microRNA-28-5p (miR-28-5p), which resulted in the upregulation of the miR-28-5p target P21-activated kinase 2 (PAK2). Rescue experiments revealed that the suppression of miR-28-5p expression or the overexpression of PAK2 abrogated the effects of LINC01006 downregulation on malignant cellular functions in cervical cancer. On the whole, the present study demonstrates that LINC01006 exhibits tumor-promoting functions in cervical cancer via the regulation of the miR-28-5p/PAK2 axis. These findings may provide the basis for the identification of LINC01006-targeted clinical therapy.

Non-small-cell lung cancer (NSCLC) stands as a prevalent subtype of lung cancer, with circular RNAs emerging as key players in cancer development. This study elucidates the role of circRNA-CPA4 in NSCLC. Elevated circRNA-CPA4 expression in NSCLC lines was confirmed through qRT-PCR. Silencing circRNA-CPA4 with shRNA revealed, through CCK-8, colony formation, and flow cytometry assays, a notable constraint on proliferation and promotion of apoptosis in NSCLC cells. Subcellular localization analysis, RNA immunoprecipitation, and expression level assessments were employed to decipher the intricate interplay among miR-1183, circRNA-CPA4, and PDPK1. Results demonstrated heightened circRNA-CPA4 levels in NSCLC, and its knockdown curtailed NSCLC growth in vivo. Acting as a molecular sponge for miR-1183, circRNA-CPA4 regulated PDPK1 expression. Conversely, inhibiting miR-1183 counteracted the impact of circRNA-CPA4 silencing, reinstating NSCLC cell proliferation, and impeding apoptosis. Overall, this study unveils a novel mechanism: circRNA-CPA4 promotes PDPK1 expression by sequestering miR-1183, fostering NSCLC cell proliferation, and hindering apoptosis.

Background Osteosarcoma (OS) is the most common bone cancer mostly seen in people aged 10–25 years. This research aims to clarify the function of hsa_circ_0001982 in osteosarcoma (OS) and its effect on drug resistance, preliminarily exploring its mechanism. Methods The expression of hsa_circ_0001982 and miR‐143 in OS clinical tissues and cells was detected by real‐time fluorescence quantitative polymerase chain reaction (qRT‐PCR), MTT, colony formation assay, and transwell assay assessed cell proliferation, colony formation, migration, and invasion, respectively. The targeted relationship of hsa_circ_0001982 and miR‐143 was verified by a dual‐luciferase reporter assay. Result The expression of hsa_circ_0001982 was significantly increased in OS tissues and cells (MG63), as in well as chemoresistant OS tissues and cells (MG63/Dox). Overexpression of hsa_circ_0001982 promoted proliferation, colony formation, migration, invasion, and multidrug resistance in MG63 cells. By contrast, knockdown of hsa_circ_0001982 markedly reduced the resistance of MG63/Dox cells to doxorubicin (IC50 evidently reduced). Bioinformatic prediction showed that miR‐143 was a target miRNA of hsa_circ_0001982, and a dual‐luciferase reporter assay proved this. Further experiments revealed that miR‐143 expression was notably downregulated in OS tissues, chemoresistant OS tissues, and MG63/Dox cells. Moreover, miR‐143 was negatively correlated with hsa_circ_0001982 in OS cells and tissues. Conclusion The regulation of malignant behaviors such as proliferation, invasion, migration, and multidrug resistance of OS cells by hsa_circ_0001982 may be achieved by targeting miR‐143. Moreover, hsa_circ_0001982 is a potential target for early diagnosis and targeted therapy of OS. Has_circ_0001982 was significantly overexpressed in OS tissues and cells, as well as chemotherapy‐resistant OS tissues and cells. Functionally, hsa_circ_0001982 can promote the development of OS cell proliferation, colony formation, invasion, migration, and multidrug resistance, which may be achieved by targeted inhibition of miR‐143 expression. Therefore, hsa_circ_0001982 can be used as a potential target for early diagnosis and targeted therapy of OS.

Yue X, Wang Z. Cancer Manag Res. 2020;12:7539-7552. The Editor and Publisher of Cancer Management and Research wish to retract the published paper. Concerns were raised over alleged image duplication in Figure 1I with similar images from unrelated articles, specifically: Figure 1I, panel MDA-MB-231 si-LINC00922 appears to have been duplicated with similar images in Figure 4B from Li et al, 2019 (https://doi.org/10.18632/aging.102563) and Figure 5C from Zhang et al, 2020 (https://doi.org/10.2147/CMAR.S269774). The authors responded to our queries but were unable to provide a satisfactory explanation for the alleged duplication and could not provide satisfactory original data for their study. The Editor advised for the article to be retracted. Our decision-making was informed by our policy on publishing ethics and integrity and the COPE guidelines on retraction. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as \"Retracted\". This retraction relates to this paper

Powdered cellulose (PC) and microcrystalline cellulose (MCC) show considerable different behavior during wet-extrusion and spheronization. While MCC is an appropriate pelletization aid, PC is not suitable. The differences were explained by either the “molecular-sponge” or the “crystallite-gel” hypothesis. To elucidate the differences in functionality, the effect of several polar solvents on liquid–solid interaction with PC and MCC was investigated. In addition, PC was homogenized via high pressure homogenization to reduce particle size without affecting the degree of polymerization. Mixer torque rheometry (MTR), laser diffraction and texture analysis were used to characterize the behavior of PC and MCC in wet pastes, suspensions and pellets. PC and MCC interacted differently with solvents like dimethyl sulfoxide, dimethylformamide and several glycols during MTR experiments. While PC mainly swells in appropriate solvents, MCC showed a particle size reduction, partly into colloidal dimensions. Solvents that induced liberation of colloidal fibers, also enabled a wet-extrusion/spheronization process. The quantity of colloidal cellulose only had minor effect on the resulting pellet quality. Also, the properties of the used solvent had only minor impact on the pellet size, shape and mechanical stability. PC contained small amounts of colloidal fibers after high pressure homogenization. With this pre-treated PC, wet-extrusion/spheronization process was also possible although the pellet quality is inferior to MCC pellets. Colloidal cellulose fibers have a major impact on the behavior of wet mass and on the feasibility for pellet production via wet-extrusion/spheronization. These insights provide new evidence for the “crystallite-gel” model.Graphic abstract

Glioblastoma multiforme (GBM), the most common and aggressive primary brain tumor in adults, is the most malignant and still has no cure. However, the novel role of long non-coding RNAs (lncRNAs) in the pathogenesis of glioblastoma is attracting extensive attention. LncRNAs are transcribed RNA molecules over 200 nucleotides long that do not encode proteins. Unlike small non-coding RNAs, such as microRNAs (miRNAs), lncRNAs have more complex secondary and tertiary structures that enable them to interact with DNA, RNA, and proteins and perform multiple regulatory functions. LncRNAs act as molecular sponges, absorbing and sequestering other biomolecules, particularly miRNAs, thereby preventing these molecules from performing their normal functions. LncRNAs influence glioblastoma through gene expression regulation, molecular sponge capacity, epigenetic modulation, and signaling pathway interactions. In glioblastoma, a large number of lncRNAs have been found to be abnormally expressed, affecting tumor growth, invasion and resistance to treatment. Due to its regulatory role and disease-specific expression patterns, lncRNA has become a potential biomarker for glioblastoma and a promising new therapeutic target. This paper discusses the spongy role of lncRNAs in glioblastoma and its potential therapeutic applications, which will lay a foundation for our understanding of glioblastoma biology and the development of new diagnostic and therapeutic strategies in the future.

Long intergenic non-coding RNA 922 (LINC00922) plays a critical role in the progression of lung cancer. In this study, we aimed to quantify LINC00922 expression in breast cancer and determine its influence on the malignant behavior of breast cancer cells in vitro and in vivo. We also investigated the mechanism by which LINC00922 affects the progression of breast cancer. Reverse transcription-quantitative polymerase chain reaction was performed to quantify LINC00922 expression in breast cancer tissues and cell lines. The cell counting kit-8 assay, flow cytometry, Transwell migration and invasion assays, and tumor model assays were performed to determine the effects of LINC00922 deficiency on breast cancer cell proliferation, apoptosis, migration and invasion in vitro, and tumor growth in vivo, respectively. Furthermore, bioinformatics analysis was performed to predict the potential target microRNA of LINC00922. The prediction was further evaluated using luciferase reporter and RNA immunoprecipitation assays. LINC00922 was clearly overexpressed in breast cancer tissues and cell lines. LINC00922 depletion restricted breast cancer cell proliferation, migration, and invasion but induced cell apoptosis in vitro. Additionally, its knockdown evidently repressed tumor growth of breast cancer cells in vivo. Mechanistically, LINC00922 was demonstrated to serve as a molecular sponge for miR-424-5p in breast cancer cells. Furthermore, brain-derived neurotrophic factor (BDNF) was verified as a direct target of miR-424-5p in breast cancer cells, and BDNF expression was found to be positively regulated by LINC00922 through sponging miR-425-5p. Rescue experiments further revealed that the influences on breast cancer cell proliferation, apoptosis, migration, and invasion induced by LINC00922 silencing were abrogated by increasing the output of the miR-424-5p/BDNF axis. The LINC00922/miR-424-5p/BDNF pathway is implicated in the acceleration of the malignant behavior of breast cancer cells. These findings suggest that this pathway is a promising novel molecular target in breast cancer therapy.

Gastrointestinal (GI) cancer represents a major global health problem due to its aggressive characteristics and poor prognosis. Despite the progress achieved in the development of treatment regimens, the clinical outcomes and therapeutic responses of patients with GI cancer remain unsatisfactory. Chemoresistance arising throughout the clinical intervention is undoubtedly a critical barrier for the successful treatment of GI cancer. However, the precise mechanisms associated with chemoresistance in GI cancer remain unclear. In the past decade, accumulating evidence has indicated that circular RNAs (circRNAs) play a key role in regulating cancer progression and chemoresistance. Notably, circRNAs function as molecular sponges that sequester microRNAs (miRNAs) and/or proteins, and thus indirectly control the expression of specific genes, which eventually promote or suppress drug resistance in GI cancer. Therefore, circRNAs may represent potential therapeutic targets for overcoming drug resistance in patients with GI cancer. This review comprehensively summarizes the regulatory roles of circRNAs in the development of chemoresistance in different GI cancers, including colorectal cancer, gastric cancer and esophageal cancer, as well as deciphers the underlying mechanisms and key molecules involved. Increasing knowledge of the important functions of circRNAs underlying drug resistance will provide new opportunities for developing efficacious therapeutic strategies against GI cancer.