scholarly journals Possible Molecular Mechanisms for the Roles of MicroRNA-21 Played in Lung Cancer

2019 ◽  
Vol 18 ◽  
pp. 153303381987513 ◽  
Author(s):  
Qiang Wang ◽  
Linyou Zhang

Background: We aimed to find the possible molecular mechanisms for the roles of microRNA-21 underlying lung cancer development. Methods: MicroRNA-21-5p inhibitor was transfected into A549 cells. Total RNA was isolated from 10 samples, including 3 in control group (A549 cells), 3 in negative control group (A549 cells transferred with microRNA-21 negative control), and 4 in SH group (A549 cells transferred with microRNA-21 inhibitor), followed by RNA sequencing. Then, differentially expressed genes were screened for negative control group versus control group, SH group versus control group, and SH group versus negative control group. Functional enrichment analyses, protein–protein interaction network, and modules analyses were conducted. Target genes of hsa-miR-21-5p and transcription factors were predicted, followed by the regulatory network construction. Results: Minichromosome maintenance 10 replication initiation factor and cell division cycle associated 8 were important nodes in protein–protein interaction network with higher degrees. Cell division cycle associated 8 was enriched in cell division biological process. Furthermore, maintenance 10 replication initiation factor and cell division cycle associated 8 were significantly enriched in cluster 1 and micro-RNA-transcription factor-target genes regulating network. In addition, transcription factor Dp family member 3 (transcription factor of maintenance 10 replication initiation factor and cell division cycle associated 8) and RAD21 cohesin complex component (transcription factor of maintenance 10 replication initiation factor) were target genes of hsa-miR-21-5p. Conclusions: Micro-RNA-21 may play a key role in lung cancer partly via maintenance 10 replication initiation factor and cell division cycle associated 8. Furthermore, microRNA-21 targeted cell division cycle associated 8 and then played roles in lung cancer via the process of cell division. Transcription factor Dp family member 3 and RAD21 cohesin complex component are important transcription factors in microRNA-21-interfered lung cancer.

2008 ◽  
Vol 123 (11) ◽  
pp. 2616-2625 ◽  
Author(s):  
Michiko Harao ◽  
Shinya Hirata ◽  
Atsushi Irie ◽  
Satoru Senju ◽  
Tetsuya Nakatsura ◽  
...  

2020 ◽  
Vol 12 (3) ◽  
pp. 376-382
Author(s):  
Xiao Liu ◽  
Yuanlan Chen ◽  
Zhijiao Jiang

To investigate the effect and molecular mechanism of grifolin on the proliferation, transfer, and infiltration of lung cancer (LC) cells. A control group, low grifolin group, midium grifolin group and high grifolin group, anti-miRNA-NC group, anti-miRNA-1251-5p group, grifolin + miRNA-NC group, and grifolin + miRNA-1251-5p group were established based on LC A549 cells. MTT was employed to detect cellular proliferation inhibition rate; Transwell assay was used to detect cellular transfer and infiltration; Western blot was used to test Cyclin D1, cyclin-dependent kinase inhibitor 1A (p21), matrix metalloproteinase 2 (MMP-2), and matrix metalloproteinase 9 (MMP-9) protein expression; and finally RT-qPCR was employed to test miRNA-1251-5p expression. After treatment with different concentrations of grifolin, an increase in proliferation inhibition rate of A549 cells, a decrease in migrating and invading cells, a decrease in CyclinD1, MMP-2, and MMP-9 expression, an increase in p21 expression, and a decrease in miRNA-1251-5p expression in a manner of concentration dependence was observed (P < 0.05). Inhibiting miRNA-1251-5p expression led to an increase in cellular proliferation inhibition rate, a decrease in migrating and invading cells, a decrease in CyclinD1, MMP-2, and MMP-9 expression, and an increase in p21 expression (P < 0.05). Overexpression of miRNA-1251-5p reversed the inhibitory influence of grifolin on the proliferation, transfer, and infiltration of A549 cells. Grifolin likely inhibits the proliferation, transfer, and infiltration of LC A549 cells by down-regulating miRNA-1251-5p.


Parasitology ◽  
2017 ◽  
Vol 144 (6) ◽  
pp. 793-800 ◽  
Author(s):  
JINGMEI LUO ◽  
LI YU ◽  
GUANGCHENG XIE ◽  
DAN LI ◽  
MENG SU ◽  
...  

SUMMARYTrichinella spiralis (T.spiralis) muscle-larva (ML) excretory–secretory proteins (ESPs) contain antitumour-active substances. ESPs have been shown to inhibit tumour growth. To explore the effects of these proteins on small cell lung cancer cells and the possible mechanisms of their antineoplastic action, H446 SCLC cells were co-cultured with different concentrations of T. spiralis ML ESPs for 12, 24 and 48 h. Our results showed that T. spiralis ML ESPs significantly inhibited H446 cell proliferation, which was dose-and time-dependent. The results of flow cytometry testing indicate a clear apoptosis trend in H446 cells co-cultured with ESPs for 24 h. Reverse transcription polymerase chain reaction and Western blotting results showed increased expression of pro-apoptosis genes Bax, Cyt-C, Apaf-1, caspase-9 and caspase-3, compared with the negative control group, and decreased the expression of anti-apoptosis genes Bcl-2 and Livin. Our results suggest that T. spiralis ML ESPs can induce apoptosis in H446 cells through a mitochondrial pathway, which may be a mechanism of antineoplastic action in T. spiralis ML ESPs.


2018 ◽  
Vol 243 (9) ◽  
pp. 739-748 ◽  
Author(s):  
Sei Won Kim ◽  
In Kyoung Kim ◽  
Jick Hwan Ha ◽  
Chang Dong Yeo ◽  
Hyeon Hui Kang ◽  
...  

Hypoxia is a critical characteristic of solid tumors with respect to cancer cell survival, angiogenesis, and metastasis. Hyperoxic treatment has been attempted to reverse hypoxia by enhancing the amount of dissolved oxygen in the plasma. In this study, we evaluated the effects of normobaric hyperoxia on the progression of lung cancer to determine whether oxygen toxicity can be used in cancer therapy. Following a tail vein injection of the Lewis lung carcinoma cells, C57BL/6J mice were exposed to a 24-h normobaric hyperoxia/normoxia cycle for two weeks. In addition, A549 lung cancer cells were incubated in a normobaric hyperoxia chamber for a 24-h period. As a result, the size and number of tumors in the lung decreased significantly with exposure to normobaric hyperoxia in the mouse model. Cell viability, colony-forming ability, migration, and invasion all decreased significantly in A549 cells exposed to normobaric hyperoxia and the normal control group exposed to normobaric hyperoxia showed no significant damage. Oxidative stress was more prominent with exposure to normobaric hyperoxia in cancer cells. A549 cells exposed to normobaric hyperoxia showed a significantly higher cell apoptosis ratio compared with A549 cells without normobaric hyperoxia exposure and normal human lung cells (BEAS-2B cells). The Bax/Bcl-2 mRNA expression ratio also increased significantly. Changes in the key regulators of apoptosis were similar between in vivo and in vitro conditions. The p-ERK level decreased, while the p-JNK level increased, after normobaric hyperoxia exposure in A549 cells. This study demonstrated the role of normobaric hyperoxia in inhibiting lung cancer. Normal tissue and cells showed no significant hyperoxic damage in our experimental setting. The anti-tumor effect of normobaric hyperoxia may due to the increased reactive oxygen species activity and apoptosis, which is related to the mitogen-activated protein kinase pathway. Impact statement Normobaric hyperoxia (NBO) is a feasible therapy for cancer with a low complication rate. Although NBO may be beneficial in cancer treatment, very few studies have been conducted; thus, the evidence is thin. This is the first study to clearly demonstrate morphological changes in lung cancer with NBO exposure and to investigate the underlying mechanisms both in vivo and in vitro. This study will arouse interest in NBO treatment and promote further research.


Tumor Biology ◽  
2017 ◽  
Vol 39 (3) ◽  
pp. 101042831769223 ◽  
Author(s):  
Run Shi ◽  
Qi Sun ◽  
Jing Sun ◽  
Xin Wang ◽  
Wenjie Xia ◽  
...  

The cell division cycle 20, a key component of spindle assembly checkpoint, is an essential activator of the anaphase-promoting complex. Aberrant expression of cell division cycle 20 has been detected in various human cancers. However, its clinical significance has never been deeply investigated in non-small-cell lung cancer. By analyzing The Cancer Genome Atlas database and using some certain online databases, we validated overexpression of cell division cycle 20 in both messenger RNA and protein levels, explored its clinical significance, and evaluated the prognostic role of cell division cycle 20 in non-small-cell lung cancer. Cell division cycle 20 expression was significantly correlated with sex (p = 0.003), histological classification (p < 0.0001), and tumor size (p = 0.0116) in non-small-cell lung cancer patients. In lung adenocarcinoma patients, overexpression of cell division cycle 20 was significantly associated with bigger primary tumor size (p = 0.0023), higher MKI67 level (r = 0.7618, p < 0.0001), higher DNA ploidy level (p < 0.0001), and poor prognosis (hazard ratio = 2.39, confidence interval: 1.87–3.05, p < 0.0001). However, in lung squamous cell carcinoma patients, no significant association of cell division cycle 20 expression was observed with any clinical parameter or prognosis. Overexpression of cell division cycle 20 is associated with poor prognosis in lung adenocarcinoma patients, and its overexpression can also be used to identify high-risk groups. In conclusion, cell division cycle 20 might serve as a potential biomarker for lung adenocarcinoma patients.


Animals ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 1238
Author(s):  
Román Gonzalez ◽  
Laura Elvira ◽  
Carlos Carbonell ◽  
Geert Vertenten ◽  
Lorenzo Fraile

Neonatal calf diarrhoea (NCD) is a major health challenge with a negative impact on farm profitability, calf welfare and antimicrobial use. Neonatal calves are particularly sensitive to enteric infections. Thus, a key point for prevention is minimising infectious pressure and maximising specific immune responses. An amount of 120 dams not previously vaccinated against NCD were randomly allocated to one of three study groups: negative control versus two vaccinated groups (A and B). In the control group, the average level of antibodies was significantly low for both BoCV and ETEC (15.6 and 13.9% in the colostrum samples, respectively), demonstrating the importance of dam vaccination. Indeed, the level of specific immunity was significantly increased for BoCV and ETEC with dam vaccination using both one-shot vaccines versus the control group. Moreover, the statistical analysis revealed a significantly higher level of antibodies for BoCV and ETEC in colostrum samples in vaccine A versus vaccine B and the control group. In accordance, the calf serum demonstrated a significantly higher level and greater homogeneity of antibodies against BoCV and ETEC in the Vaccine A group versus other experimental groups (p < 0.05). In conclusion, this study demonstrated a different specific immune response for the pathogens depending on the vaccine used to control NCD in cows.


2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Chu Huang ◽  
Weiming Yue ◽  
Lin Li ◽  
Shuhai Li ◽  
Cun Gao ◽  
...  

Objective. This Work is aimed at exploring the effect of microRNA (MiR)-608 on the function of nonsmall cell lung cancer (NSCLC) A549 cells and related mechanisms. Methods. Blood samples of 106 NSCLC patients (experimental group) as well as 124 normal people (control group) were selected for relevant investigation. Polymerase chain reaction (PCR) as well as DNA sequencing was used to determine the genotyping of the MiR-608 rs4919510 polymorphism. MiR-608 expression in cells was detected by real-time PCR technology. Western blotting was used to detect changes in protein levels. NSCLC tissues as well as adjacent tissues were explored in 33 patients undergoing surgery. Results. MiR-608 rs4919510 does not influence the incidence of NSCLC patients. In addition, MiR-608 expression was downregulated in the tumor tissue of NSCLC patients, while the transcription factor activating enhancer-binding protein 4 (TFAP4) expression was upregulated. MiR-608 promotes DOX- (Doxorubicin-) induced apoptosis by negatively regulating TFAP4 expression in NSCLC tissue. TFAP4 can significantly inhibit the migration of A549 cells. Conclusion. The findings in this investigation can contribute to the effective treatment of NSCLC patients. Also, the investigation can provide some theoretical support for the application of new targets for NSCLC treatment.


2020 ◽  
Vol 12 (9) ◽  
pp. 1099-1105
Author(s):  
Li Wei ◽  
Lijun Liu ◽  
Lin Chen ◽  
Xiaoning Li ◽  
Zaiyan Wang ◽  
...  

This study investigated whether long noncoding RNA interfering EIF3J antisense RNA1 (EIF3JAS1) could affect lung cancer A549 cells as well as the role of microRNA-330-5p (miR-330-5p) during this process. To this end, quantitative real-time polymerase chain reaction was used to measure EIF3J-AS1 and miR-330-5p expression in 39 lung cancer cases. Small interfering RNA targeting EIF3J-AS1 (si-EIF3J-AS1), as well as the miR-330-5p inhibitor, was transfected into lung cancer A549 cells. The outcomes of cell proliferation, clone formation, migration, invasion, and E- and N-cadherin expression were analyzed using CCK-8 kit, clone formation experiment, Transwell method, and Western blot. The targeted binding between EIF3J-AS1 and miR-330-5p was explored using the luciferase experiment. The results showed higher EIF3J-AS1 expression but lower miR-330-5p expression cancer tissues. Furthermore, interfering EIF3J-AS1 increased miR-330-5p and E-cadherin protein expression, leading to a reduction in the proliferation, clone formation, migration, invasion, and N-cadherin protein expression of lung cancer A549 cells. Meanwhile, Transfecting si-EIF3J-AS1 and the miR-330-5p inhibitor could increase the proliferation, clone formation, migration, invasion, and N-cadherin protein expression of lung cancer A549 cells, suggesting the targeted relationship of EIF3J-AS1 to miR-330-5p. In summary, EIF3J-AS1 was highly expressed in lung cancer tissues, and interfering EIF3J-AS1 inhibited the proliferation,migration, and invasion of A549 cells through negative regulation of miR-330-5p.


Sign in / Sign up

Export Citation Format

Share Document