Background & Aims Noncoding RNAs (ncRNAs) play critical roles in hepatocellular carcinoma (HCC) progression. Here, by performing RNA‐sequencing (RNA‐Seq) profiling, we sought to identify novel ncRNAs that potentially drive the heterogeneous progression of liver cancers. Methods RNA‐Seq profiles were obtained from 68 HCC specimens and 10 samples of adjacent non‐tumour liver tissues. The functional significance of the potential driver ncRNAs was evaluated by cell experiments. Results TPRG1‐AS1 was identified as a potential driver noncoding RNA that promotes heterogeneous liver cancer progression. TPRG1‐AS1 induced tumour suppressor RNA‐binding motif protein 24 (RBM24), suppressing tumour growth by activating apoptotic tumour cell death. In addition, we report that TPRG1‐AS1 acts as a competing endogenous RNA (ceRNA) for RBM24, sponging miR‐4691‐5p and miR‐3659 to interfere with their binding to RBM24. Conclusions We suggest that TPRG1‐AS1 is a novel ceRNA sponging miR‐4691‐5p and miR‐3659, resulting in RBM24 expression and suppression of liver cancer growth. Our results provide new insights into the functions of ncRNAs in heterogeneous HCC progression.

Alternative splicing of RNA transcripts plays an important role in cancer development and progression. Recent advances in RNA-seq technology have made it possible to identify alternately spliced events in various types of cancer; however, research on hepatocellular carcinoma (HCC) is still limited. Here, by performing RNA-Seq profiling of HCC transcripts at isoform level, we identified tumor-specific and molecular subtype-dependent expression of the USO1 isoforms, which we designated as a normal form USO1-N (XM_001290049) and a tumor form USO1-T (NM_003715). The expression of USO1-T, but not USO1-N, was associated with worse prognostic outcomes of HCC patients. We confirmed that the expression of USO1-T promoted an aggressive phenotype of HCC, both in vitro and in vivo. In addition, structural modeling analyses revealed that USO1-T lacks an ARM10 loop encoded by exon 15, which may weaken the dimerization of USO1 and its tethering to GM130. We demonstrated that USO1-T ensured unstacking of the Golgi and accelerated the trafficking from ER to Golgi and plasma membrane in multiple liver cancer cells. ERK and GRASP65 were found to be involved in the USO1-T mediated Golgi dysfunction. Conclusively, we provide new mechanophysical insights into the USO1 isoforms that differentially regulate the ER-Golgi network, promoting the heterogeneous HCC progression.

Sex/gender disparity has been shown in the incidence and prognosis of many types of diseases, probably due to differences in genes, physiological conditions such as hormones, and lifestyle between the sexes. The mortality and survival rates of many cancers, especially liver cancer, differ between men and women. Due to the pronounced sex/gender disparity, considering sex/gender may be necessary for the diagnosis and treatment of liver cancer. By analyzing research articles through a PubMed literature search, the present review identified 12 genes which showed practical relevance to cancer and sex disparities. Among the 12 sex-specific genes, 7 genes ( BAP1 , CTNNB1 , FOXA1 , GSTO1 , GSTP1 , IL6 , and SRPK1 ) showed sex-biased function in liver cancer. Here we summarized previous findings of cancer molecular signature including our own analysis, and showed that sex-biased molecular signature CTNNB1 High , IL6 High , RHOA High and GLIPR1 Low may serve as a female-specific index for prediction and evaluation of OS in liver cancer patients. This review suggests a potential implication of sex-biased molecular signature in liver cancer, providing a useful information on diagnosis and prediction of disease progression based on gender.

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The purpose of this study is to present four case reports on the treatments of psoriasis initiated after acute tonsillitis. Methods: We administered herbal medicine to four patients who showed psoriasis symptoms after acute tonsillitis and evaluated the results by Psoriasis Area and Severity Index(PASI).