LncRNA TINCR/microRNA-107/CD36 regulates cell proliferation and apoptosis in colorectal cancer via PPAR signaling pathway based on bioinformatics analysis.

The present study aims to determine the potential biomarkers and uncover the regulatory mechanisms of the long-noncoding RNA (lncRNA) TINCR/miR-107/CD36 axis in colorectal cancer (CRC). Aberrantly-expressed lncRNAs and differential-expressed genes were identified by analyzing the dataset GSE40967. Gene set enrichment analysis was employed, and Cytoscape software helped in establishing the co-expression network between lncRNAs and genes. Quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis contributes to examining the expression levels of lncRNA TINCR, miR-107 and CD36. The dual luciferase assay was used to validate the association between miR-107 and lncRNA TINCR or CD36. The EdU incorporation assay was employed, and flow cytometry was employed to detect cell apoptosis with the tumor xenograft model being utilized. Significantly dysregulated lncRNAs and mRNAs were identified. The peroxisome proliferator-activated receptor (PPAR) signaling pathway in CRC tissues was down-regulated. The loss of TINCR expression was associated with CRC progression. The expression levels of the TINCR and CD36 were down-regulated. We identified miR-107 as an inhibitory target of TINCR and CD36. Overexpression of TINCR could inhibit cell proliferation and promote apoptosis. MiR-107 overexpression in CRC cells induced proliferation and impeded apoptosis. A regulatory function of the lncRNA TINCR/miR-107/CD36 axis in CRC was revealed. LncRNA TINCR overexpression exerted suppressive influence on CRC progression through modulating the PPAR signaling pathway via the miR-107/CD36 axis.

The influence of social exclusion on prosocial behavior of college students: the role of relational need threat and regulatory focus.

The present study investigated the impact of social exclusion on prosocial behavior, examining the roles of relational need threat and regulatory focus. Utilizing a questionnaire study with 483 participants (Study 1) and an experimental study with 100 participants (Study 2), we found that (1) social exclusion negatively predicted prosocial behavior; (2) relational need threat fully mediated the relationship between social exclusion and prosocial behavior; and (3) regulatory focus, categorized as either promotion or prevention, moderated this relationship in opposite directions. In conclusion, our findings reveal that social exclusion does indeed trigger prosocial behavior. Meanwhile, relational need threat and regulatory focus have a co-action impact on this process. These findings have been carefully discussed within the frameworks of the temporal need-threat model and the cognitive-affective personality system theory.

Hsa_circ_0026628 promotes the development of colorectal cancer by targeting SP1 to activate the Wnt/ß-catenin pathway.

Circular RNAs (circRNAs) have been reported to play crucial roles in the progression of various cancers, including colorectal cancer (CRC). SP1 (Sp1 transcription factor) is a well-recognized oncogene in CRC and is deemed to trigger the Wnt/ß-catenin pathway. The present study was designed to investigate the role of circRNAs which shared the same pre-mRNA with SP1 in CRC cells. We identified that hsa_circ_0026628 (circ_0026628), a circular RNA that originated from SP1 pre-mRNA, was upregulated in CRC cells. Sanger sequencing and agarose gel electrophoresis verified the circular characteristic of circ_0026628. Functional assays including CCK-8, colony formation, transwell, immunofluorescence staining, and sphere formation assay revealed the function of circ_0026628. RNA pull-down and mass spectrometry disclosed the proteins interacting with circ_0026628. Mechanistic assays including RIP, RNA pull-down, CoIP, ChIP, and luciferase reporter assays demonstrated the interplays between molecules. The results depicted that circ_0026628 functioned as a contributor to CRC cell proliferation, migration, EMT, and stemness. Mechanistically, circ_0026628 served as the endogenous sponge of miR-346 and FUS to elevate SP1 expression at the post-transcriptional level, thus strengthening the interaction between SP1 and ß-catenin to activate the Wnt/ß-catenin pathway. In turn, the downstream gene of Wnt/ß-catenin signaling, SOX2 (SRY-box transcription factor 2), transcriptionally activated SP1 and therefore boosted circ_0026628 level. On the whole, SOX2-induced circ_0026628 sponged miR-346 and recruited FUS protein to augment SP1, triggering the downstream Wnt/ß-catenin pathway to facilitate CRC progression.

FAM225A facilitates colorectal cancer progression by sponging miR-613 to regulate NOTCH3.

Colorectal cancer (CRC) is a fatal disease ranking the third among the commonplace cancer types around the world. It is extremely significant to exploit effective treatments against CRC. FAM225A was proved to influence cell progression and forecast unfavorable prognosis in nasopharyngeal carcinoma. The role and function mechanism of FAM225A are still unclear in CRC. In this research, FAM225A was discovered presenting much higher expression in CRC tissues and cell lines. In addition, depleting FAM225A was capable of inhibiting cell proliferation, migration, and epithelial-to-mesenchymal transition (EMT) progress, and enhancing cell apoptosis ability. Furthermore, miR-613 exerted important effects as a mediator between FAM225A and NOTCH3. NOTCH3 was negatively correlated with miR-613, whereas was positively associated with FAM225A. Via competitively binding with miR-613, FAM225A positively regulated NOTCH3 expression. FAM225A facilitated CRC occurrence and development through positively regulating NOTCH3 expression by binding with miR-613. In a word, FAM225A/miR-613/NOTCH3 axis may play a tumor-facilitator in CRC cell progression. These data manifested the pivotal effect of FAM225A/miR-613/NOTCH3 pathway in CRC cell proliferation, apoptosis, and migration process. The findings may provide some theoretical basis and different perspective for CRC treatment.