The dynamic interchange between monomeric globular actin (G-actin) and polymeric filamentous actin filaments (F-actin) is fundamental and essential to many cellular processes, including cytokinesis and maintenance of genomic stability. Here, we report that the long noncoding RNA LNC CRYBG3 directly binds G-actin to inhibit its polymerization and formation of contractile rings, resulting in M-phase cell arrest. Knockdown of LNC CRYBG3 in tumor cells enhanced their malignant phenotypes. Nucleotide sequence 228-237 of the full-length LNC CRYBG3 and the ser domain of β-actin is essential for their interaction, and mutation of either of these sites abrogated binding of LNC CRYBG3 to G-actin. Binding of LNC CRYBG3 to G-actin blocked nuclear localization of MAL, which consequently kept serum response factor (SRF) away from the promoter region of several immediate early genes, including JUNB and Arp3, which are necessary for cellular proliferation, tumor growth, adhesion, movement, and metastasis. These findings reveal a novel lncRNA-actin-MAL-SRF pathway and highlight LNC CRYBG3 as a means to block cytokinesis and to treat cancer by targeting the actin cytoskeleton. Identification of the long noncoding RNA LNC CRYBG3 as a mediator of microfilament disorganization marks it as a novel therapeutic antitumor strategy. .

Cancer cells usually utilize glucose as a carbon source for aerobic glycolysis, a phenomenon known as the Warburg effect. And a high rate of glycolysis has been observed in lung cancer cells. The growing evidence indicates that long non-coding RNAs (lncRNAs) are important players in lung cancer initiation and progression. However, the correlation between lncRNAs and glycolysis remains unclear. In this study, we recognized a lncRNA, LNC CRYBG3, which can interact with lactate dehydrogenase A (LDHA), a vital enzyme of glycolysis, is highly upregulated in both clinical lung cancer tissues and in vitro cultured lung cancer cell lines. A positive correlation between the expression level of LNC CRYBG3 and LDHA expression levels is observed. In another hand, LNC CRYBG3 is a regulator of glycolysis and its overexpression promoted the uptake of glucose and the production of lactate whereas the knockdown of LNC CRYBG3 led to opposite results and suppressed cell proliferation. These results indicated that LNC CRYBG3 might be a novel target for lung cancer treatment.

Ultraviolet (UV), particularly UVB, is widely used in the treatment of skin diseases including psoriasis, atopic dermatitis, vitiligo, mycosis fungoides and pruritus. Recently, there has been a trend of replacing broad‐band UVB (BB‐UVB) units with narrow‐band UVB (NB‐UVB), as studies have demonstrated that NB‐UVB is more efficacious in the treatment of psoriasis. The purpose of this study is to evaluate the biological effects and transcriptome changes induced by light‐emitting diode‐based NB‐UVB (NB‐UVB LED) phototherapy. Cell viability and the cell migration ability were significantly decreased posttreatment, as well as apoptosis and ROS levels were remarkably increased. NB‐UVB‐induced S phase arrest was observed 12 h postirradiation. Bioinformatics analysis of transcriptome sequencing data revealed that NB‐UVB LED irradiation induced dose‐depended changes in multiple key signaling pathways, such as PI3K and cytoskeletal‐related pathways. The depolymerization of cytoskeleton induced by NB‐UVB was observed 24 h posttreatment. In addition, the expression levels of cytoskeleton‐related proteins FN1, ITGB4, ITGA1, RAC2 and DOCK1 decreased significantly 12 h after irradiation. Our results indicated that NB‐UVB LED may serve as a novel option for the development of NB‐UVB phototherapy devices.

<p>Supplement Materials and Methods</p>