ABSTRACT
With the development and progress of society, people's average life expectancy has increased, and relevant literature reports that the number of postmenopausal women in China continues to increase. With lifespans extended, the transition period and post-menopause period have become the longest essential period in every woman's life. The life quality of women troubled by perimenopausal syndrome has been significantly reduced, which also places a burden on families and society. It is well known that hormone replacement therapy plays a vital role in improving women's menopause-related symptoms and is the most effective medical measure. With research ongoing into the treatment of menopausal symptoms in different patients, dose size, treatment duration, and medication regimens for hormones are still hot topics of discussion. This article reviews the definition, clinical diagnosis, staging, clinical manifestations, and treatment of menopause and explores the current diagnosis and treatment scenarios of perimenopausal syndrome.
ABSTRACT
Cervical cancer (CC) is a very usual reproductive malignant tumor in women. RNA polymerase II-associated factor 1 (PAF1) and flotillin-2 (FLOT2) both have been discovered to key participators in cancers' progression. However, the effects of PAF1/FLOT2 axis on CC development have not been probed. In this study, PAF1 and FLOT2 exhibited higher expression, and silencing of PAF1 down-regulated FLOT2 expression in CC. In addition, the regulatory effects of PAF1 suppression on CC progression were reversed after FLOT2 overexpression. Next, inhibition of PAF1 slowed the tumor growth in vivo through modulating FLOT2. Besides, down-regulation of PAF1 reduced FLOT2 expression to retard the MEK/ERK1/2 pathway. In conclusion, knockdown of PAF1 suppressed CC progression via retarding FLOT2-mediated MEK/ERK1/2 pathway. Our findings illustrated that the PAF1/FLOT2 axis may be useful bio-targets for CC treatment.
Subject(s)
Uterine Cervical Neoplasms , Female , Humans , Uterine Cervical Neoplasms/genetics , MAP Kinase Signaling System , Cell Proliferation/genetics , Mitogen-Activated Protein Kinase Kinases , Transcription FactorsABSTRACT
Background: As prevalent cancer in women, approximately 569,847 cases of cervical cancer occur every year. Aims: This study aimed to explore the role of FLOT2 and its related mechanism in the development of cervical cancer. Study Design: Cell culture study and animal experimentation. Methods: Quantitative reverse-transcription polymerase chain reaction PCR and Western blot analysis were performed to evaluate the expression of FLOT2. Flow cytometry was applied for the evaluation of cell apoptosis. Cell Counting Kit-8 and colony formation were utilized for proliferation measurement. Cervical cancer mice model was employed to measure the role of FLOT2 in vivo. Results: FLOT2 mRNA and protein levels were dramatically elevated (P < 0.001) in cervical cancer cell line HcerEpic cells. The cell viability and proliferation of cervical cancer cells were enhanced (P < 0.01) by overexpression of FLOT2 and reduced (P < 0.01) by FLOT2 downregulation. In addition, FLOT2 overexpression elevated (P < 0.01) the cell migration abilities of cervical cancer cells, whereas its depletion inhibited (P < 0.01) the cell migration abilities. Moreover, the protein expression of epithelial-mesenchymal transition markers including Vimentin, N-cadherin, and E-cadherin were assessed, and the results showed enhanced Vimentin and N-cadherin levels (P < 0.05) by FLOT2 upregulation and declined (P < 0.01) by FLOT2 downregulation. FLOT2 upregulation reduced (P < 0.05) the level of E-cadherin protein, whereas FLOT2 suppression attenuated this effect (P < 0.05). Furthermore, FLOT2 increased (P < 0.05) p-MEK/MEK, p-ERK1/2/ERK1/2, and p-AKT/AKT levels to activate the MEK/ERK1/2 and AKT pathways in cervical cancer. Finally, our results indicated that FLOT2 inhibited (P < 0.001) cervical cancer growth in vivo. Conclusion: FLOT2 aggravates the proliferation and epithelialmesenchymal transition of cervical cancer by activating the MEK/ ERK1/2 and AKT pathways.