The mechanism of LncRNA01977 in lung adenocarcinoma through the SDF-1/CXCR4 pathway.

Background: A significant correlation has been identified between lncRNA and tumor cell resistance, diagnosis, and prognosis. Although mRNA studies have dominated the field of non-coding RNA biology in tumorigenesis in recent years, long-chain non-coding RNA (the biological function) has also attracted increasing attention. However, the lncRNA associated with lung adenocarcinoma (LUAD) remains unexplored. This study used bioinformatics analysis to screen and identify LncRNA01977 as a key oncogenic driver of LUAD. Methods: The experiment was divided into blank serum group (normal serum medium) and lung compound low, medium and high dose groups (5%, 10%, 15% and 15% lung compound drug serum medium, respectively). Transwell invasion ability of A549 cells was detected, and Western blot tested A549 cells SDF-1 specific receptor CXCR4, and CXCR4 gene expression in A549 cells were determined by reverse transcription-polymerase chain reaction (RT-PCR). In addition, western blotting, MTT proliferation test, colony formation test and apoptosis detection techniques were used to explore the mechanism of LncRNA01977's effects on LUAD. Results: In vitro assays demonstrated that LncRNA01977 can significantly promote the progression of LUAD and that stromal cells in tumor microenvironment secrete chemokine CXCL12, also known as stromal derived factor-1 (SDF-1), and its receptor CXCR4 is low expressed in normal tissues and high expressed in LUAD tissues. Lung cancer patients with high expression of CXCR4 are more prone to metastasis. Conclusions: LncRNA01977 can be used as a new prognostic indicator of LUAD, and can help patients to find more effective target treatment options for LUAD.

Assessment of DNA Damage and Cell Senescence in Corneal Epithelial Cells Exposed to Airborne Particulate Matter (PM2.5) Collected in Guangzhou, China.

PURPOSE: To assess the genotoxic effect of airborne particulate matter on corneal epithelial cells and investigate the role of reactive oxygen species (ROS) formation in this process. METHODS: Immortalized human corneal epithelial cells (HCECs) and primary bovine corneal epithelial cells were exposed to airborne particulate matter collected from Guangzhou for 24 hours. The cell viability and toxicity were measured by the CCK-8 test and lactate dehydrogenase (LDH) release, respectively. The DNA breaks and DNA repair were examined by alkaline comet assay and by immunofluorescence staining of the phosphorylated histone variant H2AX (γH2AX), respectively. Reactive oxygen species production was assessed by the fluorescent probe, CM-H2DCFDA. Cell senescence was evaluated with senescence-associated ß-Galactosidase staining, and cell ultrastructure was observed with transmission electron microscopy. RESULTS: Exposure to PM2.5 at the concentration of 20 µg/mL to 200 µg/mL decreased cell viability and increased LDH release. Remarkably increased DNA double-stand breaks, increased expression of DNA repair-related protein γH2AX, elevated ROS formation, and altered cell ultrastructure were observed in HCECs after treatment with PM2.5. The genotoxic effect of PM2.5 was attenuated by the ROS inhibitor N-acetyl-l-cysteine (NAC). CONCLUSIONS: Particulate matter 2.5 could induce DNA damage and cell senescence in corneal epithelial cells, probably by promoting ROS formation. Thus, whether long-term exposure of PM2.5 might be related to potential risk of abnormality in corneal epithelium renewal and regeneration should be further investigated.

[Screening and identifying differentially expressed proteins in LST-R1 cells].

BACKGROUND & OBJECTIVE: Colorectal laterally spreading tumor (CLST) rarely invades deeply but always laterally spreads along the colorectal mucosa, therefore, CLST could be used as a comparative model in studying the invasion and metastasis of colorectal cancer (CRC). This study was to identify differentially expressed proteins between a CLST cell line LST-R1 and two colorectal carcinoma cell lines SW480 and LoVo using proteomic technology. METHODS: Total proteins of LST-R1, SW480 and LoVo cells were isolated by two-dimensional electrophoresis (2-DE). Differentially expressed protein spots were analyzed with Melanie 3 software. The peptide mass fingerprints (PMFs) of differently expressed proteins were analyzed by MALDI-TOF mass spectrum. Subsequently matched proteins were searched through protein databases. RESULTS: Using pH4-7 IPG gels with 250 microg protein loading, the numbers of protein spots in 2-DE maps were 1285+/-51 in LST-R1 cells, 1184+/-47 in SW480 cells, and 1124+/-54 in LoVo cells; when with 150 microg protein loading, the numbers were 989, 935 and 893, respectively. The distribution and levels of these proteins in 2-DE maps of LST-R1, SW480 and LoVo cells were analogical which indicated CLST also expresses the protein profile of common colorectal tumors. In 2-DE maps, 96+/-7 differential protein spots were detected between LST-R1 cells and SW480 cells with 50+/-6 only expressed or obviously over-expressed in LST-R1 cells and 47+/-5 in SW480 cells; 108+/-10 differential protein spots were detected between LST-R1 cells and LoVo cells with 56+/-8 only expressed or obviously over-expressed in LST-R1 cells and 52+/-11 in LoVo cells. Nineteen differentially expressed proteins were identified among LST-R1, SW480 and LoVo cells. CONCLUSION: Nineteen differentially expressed proteins are possibly involved in laterally spreading of CLST and adhesion and invasion of CRC.

[Expression of tissue inhibitor of metalloproteinase-1 in colorectal carcinoma and its clinical implications].

OBJECTIVE: To investigate the expression and clinical implication of tissue inhibitor of metalloproteinase-1 (TIMP-1) in colorectal carcinoma. METHODS: TIMP-1 expression in 54 colorectal carcinoma was observed by SP immunohistochemical method, and the results were analyzed in relation to the clinical data of patients. RESULTS: TIMP-1 was localized on the membrane and in the cytoplasm of the enteric epithelial cells, and its expression rate was 100% in normal tissue but only 59.6% (31/52) in colorectal carcinoma tissues. In addition, the expression rate of TIMP-1 was higher in the tumor tissues without lymph node metastasis than in tissues with lymph node metastasis (P<0.05). CONCLUSION: The expression of TIMP-1 is inversely correlated to lymph node metastasis of colorectal carcinoma, and decreased TIMP-1 expression may play a role in the progression of colorectal carcinoma.