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Exosomal long noncoding RNA (lncRNA) has been found to be associated with the development of cancers. However, the expression characteristics and the biological roles of exosomal lncRNAs in hepatocellular carcinoma (HCC) remain unknown. Here, by RNA sequencing, we found 9440 mRNAs and 8572 lncRNAs were differentially expressed (DE‐) in plasma exosomes between HCC patients and healthy controls. Exosomal DE‐lncRNAs displayed higher expression levels and tissue specificity, lower expression variability and splicing efficiency than DE‐mRNAs. Six candidate DE‐lncRNAs (fold change 6 or more, P ≤ .01) were high in HCC cells and cell exosomes. The knockdown of these candidate DE‐lncRNAs significantly affected the migration, proliferation, and apoptosis in HCC cells. In particular, a novel DE‐lncRNA, RP11‐85G21.1 (lnc85), promoted HCC cellular proliferation and migration by targeted binding and regulating of miR‐324‐5p. More importantly, the level of serum lnc85 was highly expressed in both Alpha‐fetoprotein (AFP)‐positive and AFP‐negative HCC patients and allowed distinguishing AFP‐negative HCC from healthy control and liver cirrhosis (area under the receiver operating characteristic curve, 0.869; sensitivity, 80.0%; specificity, 76.5%) with high accuracy. Our finding offers a new insight into the association between the dysregulation of exosomal lncRNA and HCC, suggesting that lnc85 could be a potential biomarker of HCC. Long noncoding RNAs (lncRNAs) and mRNAs are aberrantly expressed in plasma exosomes of hepatocellular carcinoma (HCC). Exosomal lncRNAs could have greater potential to serve as the biomarkers of HCC than mRNAs. Exosomal lncRNAs participate in the regulation of cell biology processes. RP11‐85G21.1 promotes proliferation of HCC cell lines by acting as a sponge of microRNA‐324‐5p.

Bone metastasis is associated with cancer‐related death in patients with prostate cancer (PCa). Long noncoding RNAs (lncRNAs) play critical roles in tumor progression of PCa. Nevertheless, the biological function of lncRNAs in PCa bone metastasis remains unclear. PCAT7 was identified as a bone metastasis‐related lncRNA via analyzing TCGA dataset. Meanwhile, PCAT7 was found to be elevated in primary PCa tissues with bone metastasis and associated with bone metastasis status and poor prognosis of patients with PCa. Functionally, our results reveal that PCAT7 overexpression promotes PCa bone metastasis in vivo, as well as migration, invasion, and EMT of PCa cells in vitro; on the contrary, PCAT7 knockdown has an inverse effect. Mechanistically, PCAT7 activates TGF‐β/SMAD signaling by upregulating TGFBR1 expression via sponging miR‐324‐5p. In turn, TGF‐β signaling forms a positive feedback loop with PCAT7 via SMAD3/SP1 complex‐induced PCAT7 upregulation. Finally, the clinical positive correlation between PCAT7 and TGFBR1 and TGF‐β signaling activity, and the negative association with miR‐324‐5p are further demonstrated in PCa tissues and clinical primary PCa cells. This study reveals a novel mechanism that is responsible for the constitutive activation of TGF‐β signaling in PCa bone metastasis, implying that PCAT7 can act as a potential therapeutic target against bone metastasis of PCa via disrupting the constitutive active loop between PCAT7 and TGF‐β signaling. lncRNA PCAT7 is upregulated in primary prostate cancer tissues with bone metastasis. PCAT7 activates TGF‐β/SMAD signaling by upregulating TGFBR1 expression via sponging miR‐324‐5p. In turn, TGF‐β signaling forms a positive feedback loop with PCAT7 via SMAD3/SP1 complex‐induced PCAT7 upregulation. This feedback loop promotes prostate cancer bone metastasis.

Endometrial cancer is a common gynaecological malignant tumour among women across the world. Circular RNAs (circRNAs) are a novel kind of non‐coding RNAs, and they can play a crucial role in multiple cancers. Nevertheless, the mechanisms of circRNAs in regulating gene expression in endometrial cancer are still unclear. Here, our work sought to focus on the role that circ_0067835 exert in progression and development of endometrial cancer cells. We observed circ_0067835 was markedly elevated in endometrial cancer. Then, changes in endometrial cancer cell (RL95‐2 and HEC‐1B) function were determined after circ_0067835 knockdown. Loss‐of‐functional assays revealed that circ_0067835 down‐regulation significantly repressed RL95‐1 and HEC‐1B cell proliferation, migration and invasion. Bioinformatics analysis, luciferase reporter experiment and RNA pull‐down assay were employed to predict and validate circ_0067835 can bind to miR‐324‐5p. Increase in miR‐324‐5p remarkably depressed the proliferation, migration and invasion of endometrial cancer cells via inhibiting high mobility group A1 (HMGA1). HMGA1 is identified as a vital prognostic biomarker in endometrial cancer. Currently, we reported circ_0067835 was positively correlated with HMGA1 in endometrial cancer. We implied that circ_0067835 was capable of sponging miR‐324‐5p and inducing its downstream target HMGA1 in vitro and in vivo. In conclusion, circ_0067835 can compete with miR‐324‐5p, resulting in HMGA1 up‐regulation, and therefore induce the development of endometrial cancer.

Cervical cancer (CC) seriously threatens the health of women. Radiation therapy (RT) is the major treatment for CC. However, the recurrent CC can acquire resistance to RT. Thus, it is necessary to find a new method for reversing RT resistance in CC. It has been reported that miR‐324‐5p can suppress the progression of multiple cancers. However, whether it can reverse resistance to RT in CC remains unclear. qRT‐PCR and Western blotting were used to detect gene and protein expression in CC cells, respectively. Cell proliferation was tested by CCK‐8 assay and colony formation assay. In addition, cell apoptosis was detected by flow cytometry. Transwell assays were performed to detect cell migration. Dual luciferase reporter assay and TargetScan were used to explore the targets of microRNA‐324‐5p (miR‐324‐5p). MiR‐324‐5p was downregulated in CC cells. Overexpression of miR‐324‐5p sensitized CC cells to RT. In addition, miR‐324‐5p mimics significantly induced apoptosis and inhibits the migration of CC cells in the presence of 137Cs ionizing radiation. Furthermore, miR‐324‐5p sensitized CC cells to ionizing radiation by targeting ELAV‐like RNA binding protein 1 (ELAVL1). MiR‐324‐5p overexpression affects the radiotherapy response of CC by targeting ELAVL1, which may serve as a new target for the treatment of CC.