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Objective: Preeclampsia is a common and serious pregnancy complication, with a high risk of onset in clinical practice, which seriously affects the physical and mental health of patients. Insufficient nutrition is considered as one of the factors contributing to the occurrence of preeclampsia, but there are few reports on the prevention of preeclampsia through nutritional interventions. This study reports the effects of personalized nutritional support on a second pregnancy in a woman with severe preeclampsia. Methods: A patient with familial inherited nephropathy was followed up postpartum, and nutritional interventions including light diet, avoid spicy food, according to the principle of carbohydrate accounting for 55%-65%, fat accounting for 20%-30%, protein accounting for 10%-15%, were performed according to her individual circumstances after her second pregnancy. Moreover, the kidney function index was detected regularly by quantitative detection of urine protein in the course of pregnancy, and the pregnancy status was observed. Results: After the nutritional intervention, the 24 h urinary protein quantification and plasma albumin were decreased with the increase of gestational age, while urinary occult blood was progressive negative conversion, indicating that the kidney function of the pregnant woman gradually recovered but did not reach the normal level. Moreover, the fetal development was normal. Conclusion: Dietary nutrition treatment during pregnancy and active cooperation during pregnancy can effectively prevent the recurrence of preeclampsia in high-risk pregnant women. However, further research or larger studies are still needed to validate these findings.
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BACKGROUND: Cervical cancer (CC) is a common gynecological tumor that affects women's health. Circular RNA hsa_circ_0084927 (hsa_circ_0084927) has been reported to be upregulated in CC. However, the role and regulatory mechanism of hsa_circ_0084927 in CC are unclear. METHODS: Expression of hsa_circ_0084927, microRNA (miR)-634, and tumor protein D52 (TPD52) mRNA in CC tissues and cells was examined by quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation, colony formation, cell cycle progression, apoptosis, migration, and invasion of CC cells were determined with cell counting kit-8 (CCK-8), plate clone, flow cytometry, or transwell assays. The levels of cyclin D1, cleaved-caspase-3 (c-caspase 3), matrix metalloproteinase (MMP)-2, MMP-9, and TPD52 protein were evaluated with Western blotting. The targeting relationship between hsa_circ_0084927 or TPD52 and miR-634 was verified via dual-luciferase reporter and/or RNA immunoprecipitation (RIP) assays. Xenograft assay was conducted to confirm the role of hsa_circ_0084927 in vivo. RESULTS: Hsa_circ_0084927 and TPD52 were upregulated while miR-634 was downregulated in CC tissues and cells. Hsa_circ_0084927 silencing reduced tumor growth in vivo and induced cell cycle arrest, apoptosis, and curbed proliferation, colony formation, migration, and invasion of CC cells in vitro. Hsa_circ_0084927 regulated TPD52 expression through sponging miR-634. MiR-634 inhibitor reversed hsa_circ_0084927 knockdown-mediated impact on the malignancy of CC cells. TPD52 elevation abolished the repressive influence of miR-634 mimics on the malignancy of CC cells. CONCLUSION: Hsa_circ_0084927 accelerated CC advancement via upregulating TPD52 via sponging miR-634, offering a new evidence to support hsa_circ_0084927 as a promising target for CC treatment.
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OBJECTIVE: This research aimed to investigate the role and mechanism of long noncoding RNA (lncRNA) HCP5 in skin cutaneous melanoma (SKCM). MATERIALS AND METHODS: Survival analysis was performed using The Cancer Genome Atlas (TCGA)-SKCM data and SKCM patients' clinical data. Primary SKCM cells were derived from patients' pathologic tissue specimens. HCP5 overexpression was achieved by lentiviral transduction. Malignancy of SKCM cells was evaluated in vitro by cell proliferation, colony formation, apoptosis and transwell invasion assays. RARRES3 knockdown was achieved by siRNA transfection. DIANA microT-CDS algorithm was used to predict miRNAs that might interact with HCP5 and 3' untranslated region of RARRES3 mRNA. microRNA target luciferase reporter assay and AGO2-RNA immunoprecipitation were used to verify the interaction between HCP5, 3' UTR of RARRES3 mRNA and miR-1286. RESULTS: HCP5 level was decreased in SKCM tissue specimens compared to noncancerous counterparts. Low expression of HCP5 was associated with SKCM patients' poor overall survival and disease progression. HCP5 overexpression significantly reduced the malignancy of primary SKCM cells in vitro. RARRES3 was found as a HCP5-co-expressing gene in SKCM cells. HCP5 overexpression significantly increased RARRES3 expression in SKCM cells. RARRES3 knockdown partially abolished the anti-SKCM effect of HCP5 overexpression. MiR-1286 was found interacting with both HCP5 and 3' UTR of RARRES3 mRNA. CONCLUSION: HCP5 is a cancer-suppressive lncRNA in SKCM. HCP5 overexpression decreased SKCM cell malignancy in vitro by upregulating RARRES3, possibly via sponging miR-1286.
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Ovarian cancer is among the most prevalent and lethal types of cancers in women. Several factors such as late diagnosis, unavailability of the reliable biomarkers, frequent relapses and dearth of efficient therapeutic targets form bottleneck in the treatment of ovarian cancers. In this study we investigated the potential of less studied miR-299-3p as the therapeutic target for the treatment of ovarian cancer. The results of the present investigation revealed that miR-299 is significantly upregulated in the ovarian cancers and suppression of its expression inhibits the proliferation by induction of apoptosis as well suppresses migration and invasion of the SKOV3 cancers cells. Further, OCT-4 was found to be putative target of miR-99-3p in ovarian cancer and inhibition of OCT-4 had similar effects as that of miR-299 inhibition on cell migration and invasion. Intriguingly, even overexpression of miR-299-3p could not rescue the effects of OCT-4 suppression on SKOV3 cell proliferation, migration and invasion. On contrary, overexpression of OCT-4 in SKOV3 cells transfected with miR-299-3p transfected could nullify the effects of miR-200-3p on proliferation, migration and invasion of the SKOV3 cells. Taken together, miR-299-3p regulated cell proliferation and metastasis by modulating the expression of OCT-4 and as such may prove to be an important therapeutic target.
