Biotechnology and Genetic Engineering Reviews

LINC02489 with m6a modification increase paclitaxel sensitivity by inhibiting migration and invasion of ovarian cancer cells

The long non-coding RNA LINC02489 has been shown to be significantly downregulated in advanced ovarian cancer (OC). However, the function of LINC02489 remains unknown. This study aims to explain the role and mechanism of LINC02489 in OC. The expression of LINC02489 was examined by qRT-PCR in primary OC tissues. Additionally, MTT, wound healing, transwell, and flow cytometry assays were used to analyze the function of LINC02489. The mechanism of LINC02489 in OC was investigated by high-throughput RNA-sequencing, qRT-PCR, western blot, and N6-methyladenosine (m6A) meRIP. A total of 1101 and 827 genes are significantly down-regulated and up-regulated in metastatic and chemoresistant OC tissues. The expression of LINC02489 is decreased in metastatic and chemoresistant OC tissues compared with the primary OC tissues (

Bioinformatics analysis illustrates the functions of miR-377-5p in cervical cancer

Cervical cancer (CC) is a frequent disease in women whose development is related with miRNA disorder. MiR-377-5p plays a negative role in the development of some tumors, while few studies have revealed its role in CC. In this study, the functions of miR-377-5p in CC were investigated by bioinformatics. Briefly, the expression and survival curve of miR-377-5p in CC was analyzed with the Cancer Genome Atlas (TCGA) database, and the abundance of miR-377-5p in clinical samples and CC cell lines were measured by qRT-PCR. Moreover, the MicroRNA Data Integration Portal (miRDIP) database was used to predict targets of miR-377-5p, and the Database for Annotation Visualization and Integrated Discovery (David) was used for enrichment analysis of the functions of the miR-377-5p. The Search Tool for the Retrieval of Interacting Genes (STRING) database was used to screen the hub targets of miR-377-5p. Moreover, the Gene Expression Profiling Interactive Analysis (GEPIA) database was used to analyze the abundance of the genes in CC. Results showed that decreased miR-377-5p was found in the CC tissues and cell lines, and low miR-377-5p was connected with poor prognosis of patients. Besides, the targets of miR-377-5p were enriched in the PI3K/AKT, MAPK and RAS signaling pathways. Moreover, CDC42, FLT1, TPM3 and CAV1 were screened as hub nodes in the targets of miR-377-5p, and increased CDC42, FLT1, TPM3 and CAV1 also indicated the poor survival rates of the patients in the long term. In conclusion, this study suggests that miR-377-5p downregulation is a biomarker event for CC progression.

Study on the effect and mechanisms of piperine against cervical cancer based on network pharmacology and experimental validation

Piperine has immunomodulatory and anti-inflammatory properties, and its potential in treating cervical cancer needs further exploration. Using data from The Cancer Genome Atlas (TCGA), we identified immune-related differentially expressed genes (IRDEGs) in cervical cancer. Predicted targets of piperine were compared with cervical cancer-associated genes from various databases. Protein-protein interaction (PPI) network analysis, enrichment of GO and KEGG pathways, and molecular docking were performed. Kaplan-Meier survival analysis was done to assess prognostic significance. In vitro and in vivo experiments were conducted to confirm findings. We obtained 403 IRDEGs, 125 piperine targets, and 7037 cervical cancer genes. PPI network analysis revealed potential targets and pathways regulated by piperine. Molecular docking showed good binding activity of piperine with specific targets. In vitro, piperine inhibited cervical cancer cell proliferation, migration, and invasion, and promoted apoptosis. In vivo, piperine suppressed tumor growth and downregulated expression of IL-1β and NLRP3 in tumor cells. Piperine also downregulated expression of IL-17A, IL-21, IL-22, and RORγt, and decreased the number of Th17 cells in tumor tissues. Piperine may inhibit cervical cancer progression through modulation of Th17 cell activation mediated by the NLRP3/IL-1β axis. Further studies are warranted to explore the potential of piperine as an immunomodulatory agent in cervical cancer treatment.

Expression of ALDH1 plays the important role during generation and progression in human cervical cancer

Cervical cancer which is caused by persistent infection with oncogenic human papillomavirus (HPV), is the third most common cancer. HPV infection causes the progression of the normal cervix to cervical intraepithelial neoplasia (CIN) because it often occurs at the function conversion of the cervical squamous epithelium and columnar epithelium zone, further to invasive carcinoma. The difference in the ALDH1 expression was very significant. With the progression of cervical cancer, reports explained obviously increased nuclear and cytoplasm ALDH1 staining in comparisons of cervical carcinomas and normal cervix (P 0.05) between the ALDH1-positive groups in 100 cervical cancer tissues. But after the control variable age, different ALDH rating survival function contrasted, it can be concluded that the higher ALDH1 scores with the survival of patients with the worse condition.

Maximal clique centrality and bottleneck genes as novel biomarkers in ovarian cancer

Ovarian cancer (OC) is second most common form of gynaecological cancer world wide . In this study, we collected and analyzed three ovarian cancer microarray raw datasets from Gene Expression Omnibus, NCBI, and identified a total of 1806 significant DEGs (Differentially expressed genes). The functional analysis of the DEGs showed that the 885 upregulated DEGs were mostly enriched in protein-binding activity, while the downregulated 796 genes were mostly enriched in retinal dehydrogenase activity and GABA receptor binding. We then constructed a protein-protein interaction network of the DEGs DEGs in ovarian cancer datasetsand analyzed the network to find cluster subnets, using molecular complex detection (MCODE). Common genes among top hub gene list, bottleneck gene list and maximum clique centrality (MCC) gene lists were identified as key driver genes, After analyzing the network. The following genes, STK12 (Serine threonine protein kinase), UBE2C (Ubiquitin-conjugating enzyme E2 C), CENPA (Centromere protein A), CCNB1 (Cyclin B1), POLD1 (polymerase delta 1) and KIF11 (Kinesin Family Member 11) were finally identified as driver genes. Higher expression of the key driver genes, STK12, UBE2C, CENPA, CCNB1, POLD1 and KIF11, was associated with lower overall survival (OS) among ovarian cancer patients. Therefore, the identified driver genes could be important diagnostic and prognostic biomarkers for predicting ovarian cancer progression and understanding the mechanism of tumour formation and recurrence.

Cinobufacini suppresses malignant behaviors of endometrial cancer by regulating NF-κB pathway

Cinobufagin has inhibitory effects on various tumors, but there are few studies on gynecological tumors. This study explored the function and molecular mechanism of cinobufagin in endometrial cancer (EC). Different concentrations of cinobufagin treated EC cells (Ishikawa and HEC-1). Clone formation, methyl thiazolyl tetrazolium (MTT), flow cytometry, and transwell assays were used to detect malignant behaviors. A Western blot assay was performed to detect protein expression. Cinobufacini was sensitive to the inhibition of EC cell proliferation in a time- and concentration-dependent manner. Meanwhile, EC cell apoptosis was induced by cinobufacini. In addition, cinobufacini impaired the invasive and migratory abilities of EC cells. More importantly, cinobufacini blocked the nuclear factor kappa beta (NF-κB) pathway in EC by inhibiting p-IkBα and p-p65 expression. Cinobufacini suppresses malignant behaviors of EC by blocking the NF-κB pathway.

Hysterectomy or/and lymphadenectomy for the survival of patients with primary endometrial cancer: a cohort study using the SEER database

In order to provide a clinical reference for endometrial cancer treatment, this retrospective cohort study aimed to assess and compare the survival of endometrial cancer patients undergoing hysterectomy versus lymphadenectomy and hysterectomy combined with lymphadenectomy. The Surveillance, Epidemiology, and End Results (SEER) database provided data on patients with primary endometrial cancer enrolled between 1975 and 2016. The longest follow-up time was ten years, and the median follow-up time was 51.00 months. The outcomes were overall survival (OS) and cancer-specificsurvival (CSS). COX models were constructed to assess the relationship between the three surgical methods and OS or CSS. Subgroup analyses were conducted based on American Joint Committee on Cancer (AJCC) stage and menopausal status. Totally 134,597 patients were included. In stage IV, the lymphadenectomy group had significantly worse OS than the hysterectomy group (HR = 1.330, 95%CI = 1.101-1.606). The hysterectomy combined with lymphadenectomy group had similar OS to the hysterectomy group (HR = 1.183, 95%CI = 0.996-1.405). Regarding CSS, no significant differences were found between the hysterectomy and lymphadenectomy groups (HR = 1.267, 95%CI = 0.996-1.610), and between the hysterectomy and hysterectomy combined with lymphadenectomy groups (HR = 1.186, 95%CI = 0.953-1.476) in stage IV. For postmenopausal women, lymphadenectomy (HR = 1.655, 95%CI = 1.495-1.831) and hysterectomy combined with lymphadenectomy (HR = 1.129, 95%CI = 1.038-1.228) were associated with significantly decreased OSthan hysterectomy. For CSS among postmenopausal women, significant declines inCSS were found in the lymphadenectomy (HR = 2.264, 95%CI = 1.957-2.619) and hysterectomy combined with lymphadenectomy (HR = 1.419, 95%CI = 1.260-1.599) groups versus the hysterectomy group. Hysterectomy may serve as a decision-making reference for clinicians in treating patients in stage IV or after menopause, combined with clinical experience and patients' wishes.

A meta-analysis of the effect of pelvic and para-aortic lymph node dissection on the prognosis of patients with endometrial cancer

Endometrial cancer (EC) is the second most common malignant tumor of the female reproductive system, and it occurs in the peri- and post-menopausal periods. The metastasis routes of EC include direct spread, hematogenous metastasis and lymph node metastasis. Symptoms such as vaginal discharge or irregular vaginal bleeding may occur in the early stage. The pathological stage of the patients treated at this time is mostly in the early stage, and comprehensive treatment such as surgery, radiotherapy and chemotherapy can improve the prognosis. This article investigates whether endometrial cancer requires pelvic and para-aortic lymph node dissection. The clinical data of 228 patients with endometrial cancer who underwent pelvic lymphadenectomy in our hospital from July 2020 to September 2021 were retrospectively analyzed. All patients underwent preoperative clinical staging and postoperative pathological staging. This paper compared lymph node spread rates of endometrial carcinoma in different stages, depth of muscle invasion, and pathological characteristics to analyze lymph node metastasis risk factors. Results showed metastasis rates of 7.5% in 228 cases of endometrial cancer, increasing with deeper myometrial invasion. Different clinicopathological factors had varying lymph node spread rates. Different clinicopathological factors have different pelvic lymph node spread rates in surgical patients. The lymph node spread rate of differentially differentiated carcinoma is higher than that of well-differentiated carcinoma. The lymph node spread rate of serous carcinoma is 100%, but there is no difference between the lymph node metastasis rate of special type carcinoma and adenocarcinoma. Statistical significance (