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This study investigated whether listening comprehension played a mediator role between vocabulary and reading comprehension. 127 Mandarin-speaking children were longitudinally assessed at 6;4, 6;10, 7;4, and 7;10. Data were collected in four batteries of tests implemented at the beginning of first grade (T[subscript 1]); at mid-first grade (T[subscript 2]); at the beginning of the second grade (T[subscript 3]); and at mid-second grade (T[subscript 4]). Participants' IQ, decoding, vocabulary breadth and depth knowledge were measured at T[subscript 1], listening comprehension at T[subscript 2], and reading comprehension at T[subscript 3] and T[subscript 4] respectively. Path analysis was utilized for analysis. Vocabulary breadth was found to contribute to reading comprehension via a full mediator role of listening comprehension with a lapse of 1 and 1.5 years; however, vocabulary depth directly influenced reading comprehension with the same time lapse over the effect of decoding and listening comprehension.

Alternative splicing of precursor messenger RNA (pre‐mRNA), including linear splicing and back splicing, produces multiple isoforms that lead to diverse cell fates in response to stimuli including ultraviolet radiation (UVR). Although UVR‐induced linear gene splicing has been extensively studied in skin cells, the UVR‐induced gene back‐splicing events that lead to the production of circular RNAs (circRNAs) have not been thoroughly investigated. The present study used circRNA transcriptome sequencing to screen the differentially expressed circRNAs in human keratinocytes (HaCaT) after UVA irradiation. A total of 312 differentially expressed circRNAs were found in HaCaT cells post‐UVR. Among the UVA‐induced differentially expressed circRNAs, circUBE2I—a novel circRNA formed by exons 2–6 of the UBE2I gene—was the most significantly upregulated circRNA. RT–qPCR assay further confirmed the increase of circUBE2I level in HaCaT cells after UVA irradiation or H2O2 treatment. RNase R digestion experiment revealed the stability of circUBE2I. Overexpression of circUBE2I in keratinocytes induced ferroptosis after UVA or H2O2, preventable by the ferroptosis inhibitor ferrostatin‐1. Our study provides new insights into the role of circular RNAs in UVA‐induced skin cell damage and suggests that circUBE2I could be a therapeutic target in UVR‐aroused ferroptosis in skin cells. [ABSTRACT FROM AUTHOR]

Background: RBM3 is a key RNA-binding protein that has been implicated in various cellular processes, including cell proliferation and cell cycle regulation. However, its role in cutaneous squamous cell carcinoma (cSCC) remains poorly understood., Aims: We aimed to investigate the expression levels of RNA-binding motif protein 3 (RBM3) in patients with cSCC and evaluate its effect on cell ability in cSCC and its underlying regulatory mechanisms., Methods: The expression of RBM3 in cSCC tissues and A431 cells was determined via immunohistochemistry and western blotting. Plenti-CMV-RBM3- Puro was used to overexpress RBM3. The effect of RBM3 on the proliferation ability of cSCC cells was evaluated using MTT and colony formation assay. Cell apoptosis and cell cycle were determined using flow cytometry, while the protein expressions of BAX, NF-κB, BCL2, CASPASE 3, CYCLIN B, CYCLIN E, CDK1, phosphorylated (P)-CDK1, CDK2, P-CDK2, ERK, P-ERK, P-AMPK, AKT, P-AKT, MDM2, and P53 were assessed using western blotting., Results: RBM3 expression was significantly downregulated in cSCC tissues and A431 cells. RBM3 overexpression significantly inhibited the cell proliferation and colony formation ability of A431. Notably, RNA-seq results showed that the differentially expressed genes associated with RBM3 were primarily involved in the regulation of the cell cycle, oocyte meiosis, and P53 signaling pathway, as well as the modulation of the MAPK, AMPK, Hippo, mTOR, PI3K/AKT, Wnt, FoxO, and NF-κB signaling pathways. Additionally, our findings demonstrated that overexpression of RBM3 inhibited cell proliferation and induced cell cycle arrest of cSCC through modulation of the PI3K/AKT signaling pathway., Conclusion: This study provides novel insights into the suppressive roles of RBM3 in cell proliferation and the cell cycle in cSCC and highlights its therapeutic potential for cSCC.