Aim G2 and S phase‐expressed‐1 (GTSE1) has been identified to play a vital role in several kinds of cancers, but its role in cervical cancer development remains unknown. Herein, we aimed to reveal the role and underlying mechanism of GTSE1 in cervical cancer cell growth, migration, and aerobic glycolysis. Methods GTSE1 expression levels in cervical cancer tissues and normal cervical tissues were determined by real time PCR and immunohistochemistry. Human short hairpin RNA was used to downregulate GTSE1 level in cervical cancer cells SiHa and HeLa cells. Colony formation, cell counting kit‐8, and wound‐healing assays were used for cell function evaluation. Lactate production, lactate dehydrogenase activity, and glucose concentration were tested to assess the Warburg effect. Results GTSE1 expressions at both mRNA and protein levels were significantly elevated in cervical cancer tissues compared with normal tissues. Downregulation of GTSE1 induced significant repressions in cell colony formation, viability and migration, and Warburg effect, as well as reduced expression of lactate dehydrogenase isoform A (LDHA) at mRNA and protein levels. Additionally, downregulation of GTSE1 weakened the tumorigenesis of HeLa and SiHa cells in vivo. Conclusion This study demonstrated that downregulation of GTSE1 led to significant inhibitions in cell proliferation, migration, tumorigenesis, and Warburg effect in cervical cancer by blocking the expression of LHDA.
To determine the influence of the weight of the economic effectiveness evaluation criteria of the major investments of listed enterprises, and provide new management ideas for the development of the follow-up enterprises, firstly, the financial benefit evaluation system of investment projects is analyzed and constructed, and the specific evaluation process is analyzed. Then, on this basis, the evaluation index is refined; the basic structure of BP neural network (BPNN) is introduced, and genetic algorithm is used to improve BP neural network. The cost-benefit analysis model is constructed based on the improved BPNN. The listed company A is taken as an example to analyze its development data in recent years, and then the data of 10 listed companies are taken as the research object. Matlab simulation software is used to train and verify the improved BPNN model, analyze and predict the weight value of the financial benefit index of the investment projects of these 10 companies, and then determine the index to improve the financial benefit of the investment projects. Under the analysis of the development data of listed company A in the past 10 years, it is found that the indicators of the listed company's profitability per share, debt risk operation ability, development, and growth ability in the past 10 years are in relatively stable state. The principal component analysis of its 20 secondary sub-indexes is conducted based on the four primary indicators: profitability, debt risk, operational capacity, and development and growth. A total of eight principal components including return on equity (ROE), return on assets (ROA), (total asset turnover) TATO, turnover of account receivable (AR), asset-liability ratio, interest protection multiple, income growth rate, and year-on-year rate of increase for complete assets are extracted. The average error between the final output value, the actual value, and the expected value is 0.0304 and 0.0169, respectively. The weight coefficient of the monetary benefits evaluation indicator of investment items is calculated, and the computed results show that year-on-year rate of increase for complete assets, TOTA, ROA, turnover of total capital, and ROE are important indexes in the financial benefit evaluation of investment projects. It indicates that to improve the financial benefit of investment projects of listed enterprises, it is necessary to enhance the year-over-year growth degree of total properties and ROA.
Background Cervical cancer (CC) is the third most common gynecological malignancy around the world. Cisplatin is an effective drug, but cisplatin resistance is a vital factor limiting the clinical usage of cisplatin. Enhancer of mRNA decapping protein 4 (EDC4) is a known regulator of mRNA decapping, which was related with genome stability and sensitivity of drugs. This research was to investigate the mechanism of EDC4 on cisplatin resistance in CC. Two human cervical cancer cell lines, HeLa and SiHa, were used to investigate the role of EDC4 on cisplatin resistance in vitro. The knockdown or overexpression of EDC4 or replication protein A (RPA) in HeLa or SiHa cells was performed by transfection. Cell viability was analyzed by MTT assay. The growth of cancer cells was evaluated by colony formation assay. DNA damage was measured by γH2AX (a sensitive DNA damage response marker) immunofluorescent staining. The binding of EDC4 and RPA was analyzed by immunoprecipitation. Results EDC4 knockdown in cervical cancer cells (HeLa and SiHa) enhanced cisplatin sensitivity and cisplatin induced cell growth inhibition and DNA damage. EDC4 overexpression reduced DNA damage caused by cisplatin and enhanced cell growth of cervical cancer cells. EDC4 could interact with RPA and promote RPA phosphorylation. RPA knockdown reversed the inhibitory effect of EDC4 on cisplatin-induced DNA damage. Conclusion The present results indicated that EDC4 is responsible for the cisplatin resistance partly through interacting with RPA in cervical cancer by alleviating DNA damage. This study indicated that EDC4 or RPA may be novel targets to combat chemotherapy resistance in cervical cancer. Graphical abstract
The anticancer effect of miR-1179 has been extensively studied in many tumors. The mechanism of miR-1179 action in cervical cancer, however, remains largely unknown. In the present study, miR-1179 was downregulated in both cervical cancer cell lines and cancer tissues. In addition, miR-1179 mimic suppressed cancer cells invasion and epithelial-mesenchymal transition (EMT) in cervical cancer SiHa and Caski cells. We found that chromatin assembly factor 1 subunit A (CHAF1A) might be a direct target of miR-1179 and could be regulated by miR-1179. Furthermore, CHAF1A shRNA suppressed the cervical cancer cells invasion and the expression of EMT-promoted proteins. Reversely, CHAF1A overexpression not only promoted cervical cancer cells invasion but also upregulated the level of Zinc finger E‐box binding protein 1 (ZEB1), an EMT-related protein. The induction of ZEB1 could be counteracted by miR-1179 overexpression. It was observed that in cervical cancer patients’ tissues, miR-1179 was downregulated while the pathway of CHAF1A/ZEB1 was upregulated. In summary, our research indicated that the miR-1179 might regulate CHAF1A/ZEB1 axis and inhibit the invasion of cervical cancer cells.
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