A cross-sectional study of human papillomavirus genotype distribution and integration status in penile cancer among Chinese population.

Human papillomavirus (HPV) has been recognized as an important risk factor in penile cancer. This study aimed to investigate the HPV subtypes and integration status in Chinese patients. Samples were collected from 103 penile cancer patients aged 24-90 years between 2013 and 2019. We found that HPV infection rate was 72.8%, with 28.0% integration. The aging patients were more susceptible to HPV (p = 0.009). HPV16 was the most frequent subtype observed (52/75) and exhibited the highest frequency of integration events, with 11 out of 30 single infection cases showing integration positive. The HPV integrations sites in the viral genome were not randomly distributed, the breakpoints were enriched in the E1 gene (p = 0.006) but relatively scarce in L1, E6 and E7. Our research might provide some clues how HPV leads to the progression of penile cancer.

CTHRC1 is associated with immune cell infiltration and functions as an adverse marker for prognosis in head and neck squamous cell carcinoma.

Collagen triple helix repeat containing 1 (CTHRC1) is a secreted glycoprotein that decreases the deposition of collagen matrix and accelerates tumor metastasis. However, the relationship between CTHRC1 and the outcomes of head and neck squamous cell carcinoma (HNSCC) and tumor-infiltrating lymphocytes remains unclear. In the present study, the transcriptional level of CTHRC1 and its association with overall survival (OS) and relapse-free survival (RFS) time in diverse cancer types were evaluated using The Cancer Genome Atlas, Tumor Immune Estimation Resource (TIMER), ONCOMINE and Kaplan-Meier plotter databases. The association of CTHRC1 expression level with the clinicopathological parameters of patients with HNSCC from The University of ALabama at Birmingham CANcer data analysis Portal (UALCAN) database were also evaluated. Enrichment analysis of CTHRC1 was carried out using gene set enrichment analysis software. CIBERSORT and TIMER databases were used to evaluate the relationship between the expression level of CTHRC1 and the proportion of tumor-infiltrating immune cells (TICs) in multiple cancer types. Moreover, immunohistochemistry was used to verify the expression of CTHRC1 in clinical samples of HNSCC. CTHRC1 was upregulated in HNSCC and high expression of CTHRC1 was associated with worsening clinicopathologic parameters and shorter OS and RFS times. There were eight HALLMARK gene sets, 1,231 immune signature gene sets and 14 KEGG gene sets significantly enriched in the high CTHRC1 expression group, while no gene set was enriched in the low CTHRC1 expression group. The expression of CTHRC1 was closely correlated with the proportion of TICs, where the expression of CTHRC1 was significantly positively correlated with the amount of infiltrated M0 and M2 macrophages, and significantly negatively associated with the levels of M1 macrophages. These findings suggest that CTHRC1 is an adverse prognostic marker and is associated with immune cell infiltration in HNSCC.

Role of lncRNA LINC01194 in hepatocellular carcinoma via the miR-655-3p/SMAD family member 5 axis.

Long non-coding RNAs (lncRNAs) are involved in developing hepatocellular carcinoma (HCC). The present study explored the role of lncRNA LINC01194, which is upregulated in HCC tissues and might be a vital regulator in HCC progression. Levels of LINC01194, microRNA (miR)-655-3p, and SMAD family member 5 (SMAD5) were assessed using reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR). The bioactivity of Huh-7 cells was assessed using cell counting kit-8 and transwell assays and flow cytometry. Western blotting was conducted to measure the expression of invasion- and apoptosis-related proteins. The relationships between lncRNA LINC01194 and miR-655-3p, and miR-655-3p and SMAD5 were predicted using StarBase and TargetScan, and further verified using a dual-luciferase reporter assay. LINC01194 was overexpressed in HCC cells and in clinical samples. ILINC01194 silencing suppressed proliferation and migration; however, it promoted apoptosis in HCC cell lines. We also confirmed that miR-655-3p could bind to LINC01194, and miR-655-3p was downregulated in HCC. The upregulation of miR-655-3p suppressed HCC cell invasion and migration, and enhanced the number of apoptotic cells. SMAD5, which was overexpressed in HCC cell lines, was directly targeted by miR-655-3p. Therefore, LINC01194 promoted HCC development by decreasing miR-655-3p expression and may serve as a promising therapeutic target for HCC patients.

Photoresponsiveness of Anthracene-Based Supramolecular Polymers Regulated via a σ-Platinated 4,4-Difluoro-4-bora-3a,4a-diaza-s-indacene Photosensitizer.

Anthracene and its derivatives have attracted tremendous interest in recent years because of their intriguing photoresponsive behaviors. Our research group has previously constructed anthracene-based supramolecular polymers, which display multicycle anthracene-endoperoxide photoswitching in a macroscopic manner. However, high-energy light excitation (λ = 365-460 nm) is required for anthracene-to-endoperoxide photooxygenation, giving rise to severe photodegradation problems. In this work, we have developed an effective approach to addressing this issue, by encapsulating a σ-platinated 4,4-difluoro-4-bora-3a,4a-diaza-s-indacene (BODIPY) photosensitizer into anthracene-based supramolecular polymeric systems. The platination effect enhances π-electron delocalization, while promoting intersystem crossing from singlet to triplet excited states. Accordingly, the σ-platinated BODIPY photosensitizer displays excellent 1O2 production capability, facilitating anthracene-to-endoperoxide transformation under low-energy irradiation conditions (λ = 520-590 nm). This leads to the breakup of supramolecular polymers and gels, which can be restored at room and elevated temperatures because of the reversible endoperoxide-to-anthracene deoxygenation process. Overall, the rational design of a σ-metalated photosensitizer opens up a new avenue to regulating the photoresponsiveness of supramolecular polymers under mild and nondestructive conditions.

microRNA-1225 inhibit apoptosis of pancreatic cancer cells via targeting JAK1.

The microRNA miRNA-1225-5p (miR-1225) is known as an essential modulator of the development of multiple cancers and other biological reactions. However, the understanding of its contribution to pancreatic cancer (PC) is insufficient. The effects of miR-1225 on PC cell survival and tumorigenesis in vivo as well as on the modulation of cell apoptosis were investigated. The expression of miR-1225 was upregulated in 20 human LC samples from acute myeloid leukemia patients with adverse prognosis and poor responses to therapy as well as in several human PC cell lines, as compared to that in healthy tissues, normal tissues, and normal pancreatic cells. In contrast, Janus kinase 1 (JAK1) expression was downregulated in human-derived PC samples and PC cell lines. EdU staining demonstrated that the aberrant expression of miR-1225 impaired the proliferation and survival of these two PC cell lines. The depletion of miR-1225 expression increased the apoptosis of both PANC-1 and AsPC-1 cells, as revealed by the TdT-mediated dUTP nick end labeling (TUNEL) staining and flow cytometry results. The results of dual-luciferase reporter assay indicated that miR-1225 targeted the 3'-untranslated region of JAK1 for silencing. Silencing of JAK1 expression counteracted the suppressive influence of miR-1225 depletion in PC cells. Thus, these results offer an insight into the biological and molecular mechanisms underlying the development of PC and provide potential strategies for PC treatment.

Two-component supramolecular metallogels with the presence of Pt-Pt metal-metal interactions.

Two-component supramolecular metallogels have been successfully constructed with the involvement of heteromeric Pt(ii)Pt(ii) metal-metal interactions, which display low-energy emissions in the near-infrared region. We demonstrate and rationalize how the gel stability can be increased by modulating the gelation solvent as well as the crosslinking unit.