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. 2023 Sep 9;24(18):13904.
doi: 10.3390/ijms241813904.

Novel Long Non-Coding RNA (lncRNA) Transcript AL137782.1 Promotes the Migration of Normal Lung Epithelial Cells through Positively Regulating LMO7

Ying Zhang  1   2 , Weili Wang  1   2 , Chunchun Duan  1   2 , Min Li  1   2 , Liyang Gao  1   2
Affiliations

Novel Long Non-Coding RNA (lncRNA) Transcript AL137782.1 Promotes the Migration of Normal Lung Epithelial Cells through Positively Regulating LMO7

Ying Zhang et al. Int J Mol Sci. .

Abstract

The role of long non-coding RNA (lncRNAs) in biological processes remains poorly understood, despite their significant impact. Our previous research discovered that the expression of AL137782.1, a long transcript of the novel lncRNA ENSG00000261553, is upregulated in lung epithelial cells upon exposure to microbes. Furthermore, the expression of AL137782.1 exhibits variability between para-cancerous and lung adenocarcinoma samples. These findings imply that this lncRNA may play a role in both normal lung epithelial cellular processes and pathophysiology. To elucidate the function of AL137782.1 in lung epithelial cells, we utilized bioinformatics retrieval and analysis to examine its expression. We then analyzed its subcellular localization using fluorescence in situ hybridization (FISH) and subcellular fractionation. Through rapid amplification of cDNA ends (RACE), we confirmed the presence of a 4401 nt lncRNA AL137782.1 in lung epithelial cells. Moreover, we discovered that this lncRNA positively regulates both mRNA and the protein expression of LMO7, a protein that may regulate the cell migration of normal lung epithelial cells. Although the overexpression of AL137782.1 has been shown to enhance the migration of both normal lung epithelial cells and lung adenocarcinoma cells in vitro, our study revealed that the expression of this lncRNA was significantly decreased in lung cancers compared to adjacent tissues. This suggests that the cell migration pattern regulated by the AL137782.1-LMO7 axis is more likely to occur in normal lung epithelial cells, rather than being a pathway that promotes lung cancer cell migration. Therefore, our study provides new insights into the mechanism underlying cell migration in human lung epithelial cells. This finding may offer a potential strategy to enhance normal lung epithelial cell migration after lung injury.

Keywords: LMO7; cell migration; lncRNA AL137782.1; lung epithelial cells.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Expression and relative survival rate of lncRNA AL137782.1 in lung cancer groups. (A) Expression of AL137782.1 in LUAD; (B) expression of AL137782.1 in LUSC; (C,D) patient survival rate. ** p < 0.01.
Figure 2
Figure 2
Identification of AL137782.1. (A) The position of AL137782.1 on the chromosome; (B) the open reading frame of AL137782.1; (C) prediction of the encoding capacity of AL137782.1; (D) full length of AL137782.1 ENST00000261553 was predicted in the Ensembl database and measured AL137782.1 was acquired via 5′ and 3′ RACE; (E) the result of 5′ RACE agarose gel electrophoresis; (F) lncRNA secondary structure model.
Figure 3
Figure 3
The localization of AL137782.1 in lung epithelial cells. (A,B) The subcellular localization of AL137782.1 in A549 and BEAS-2B cells was detected via RNA-FISH; (C,D) RT-qPCR was used to detect the AL137782.1 in the nucleus and cytoplasm of A549 and BEAS-2B cells.
Figure 4
Figure 4
AL137782.1 is solely co-expressed with the mRNA expression of LMO7. (A) Volcano plots show the -log10 (p value) against log2 (FC) for DEGs in lung epithelial cells, and the green, red, and gray points represent down-expressed, up-expressed, and non-DEGs, respectively (|log2FC| ≥ 1 and p value < 0.05), nosig: no significant; (B) GO enrichment analysis of DEGs; (C) KEGG pathway enrichment analysis of significantly up-regulated and down-regulates expressed genes; (D) co-expression network for AL137782.1 and its co-expressed mRNA.
Figure 5
Figure 5
Overexpressing AL137782.1 upregulates the expression of LMO7. (A) The mRNA expression of LMO7 in A549 and BEAS-2B cells were verified by means of RT-qPCR. (B) Western blot was used to verify the protein expression of LMO7 in A549 and BEAS-2B cells. (C,D) Expression of LMO7 in A549 and BEAS-2B cells was determined by means of immunofluorescence. *** p < 0.001, ns means no significant difference.
Figure 6
Figure 6
Knocking down AL137782.1 decreases the expression of LMO7. (A,B) Screening of si-AL137782.1 in A549 and BEAS-2B; (C) the mRNA expression of LMO7 in A549 and BEAS-2B cells was verified by means of RT-qPCR. (D,E) Western blot was used to verify the protein expression. (F,G) expression of LMO7 in A549 and BEAS-2B cells was determined by means of immunofluorescence. ** p < 0.01, *** p < 0.001, ns means no significant difference.
Figure 7
Figure 7
Expression and relative survival rate of lncRNA LMO7 in lung cancer groups. (A) Ex pression of LMO7 in LUAD; (B) expression of LMO7 in LUSC. *** p < 0.001.
Figure 8
Figure 8
AL137782.1 promotes the migration of lung epithelial cells. (A,B) Overexpression of AL137782.1 promoted the migration of A549 and BEAS-2B cells; (C,D) knocking down AL137782.1 suppressed the migration of A549 and BEAS-2B cells.
Figure 9
Figure 9
Knocking down LMO7 suppresses the migration of lung epithelial cell while overexpressing the expression of AL137782.1. (A) The mRNA expression of LMO7 in A549 and BEAS-2B cells were verified by RT-qPCR; (B) Western blot was used to verify the protein expression; (C,D) knocking down LMO7 suppressed the migration of A549 and BEAS-2B cells while overexpressing the expression of AL137782.1. ** p < 0.01, *** p < 0.001.
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References

    1. Guillot L., Nathan N., Tabary O., Thouvenin G., Le Rouzic P., Corvol H., Amselem S., Clement A. Alveolar epithelial cells: Master regulators of lung homeostasis. Int. J. Biochem. Cell Biol. 2013;45:2568–2573. doi: 10.1016/j.biocel.2013.08.009. - DOI - PubMed
    1. Kawakita N., Toba H., Miyoshi K., Sakamoto S., Matsumoto D., Takashima M., Aoyama M., Inoue S., Morimoto M., Nishino T., et al. Bronchioalveolar stem cells derived from mouse-induced pluripotent stem cells promote airway epithelium regeneration. Stem Cell Res. Ther. 2020;11:430. doi: 10.1186/s13287-020-01946-7. - DOI - PMC - PubMed
    1. Bhargava M., Dey S., Becker T., Steinbach M., Wu B., Lee S.M., Higgins L., Kumar V., Bitterman P.B., Ingbar D.H., et al. Protein expression profile of rat type two alveolar epithelial cells during hyperoxic stress and recovery. Am. J. Physiol. Cell. Mol. Physiol. 2013;305:L604–L614. doi: 10.1152/ajplung.00079.2013. - DOI - PMC - PubMed
    1. Becker P.M., Tran T.S., Delannoy M.J., He C., Shannon J.M., McGrath-Morrow S. Semaphorin 3A Contributes to Distal Pulmonary Epithelial Cell Differentiation and Lung Morphogenesis. PLoS ONE. 2011;6:e27449. doi: 10.1371/journal.pone.0027449. - DOI - PMC - PubMed
    1. Jansing N.L., McClendon J., Henson P.M., Tuder R.M., Hyde D.M., Zemans R.L. Unbiased Quantitation of Alveolar Type II to Alveolar Type I Cell Transdifferentiation during Repair after Lung Injury in Mice. Am. J. Respir. Cell Mol. Biol. 2017;57:519–526. doi: 10.1165/rcmb.2017-0037MA. - DOI - PMC - PubMed

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