Cervical Invasion Research Articles

Tumour texture features from preoperative CT predict high-risk disease in endometrial cancer

To enable more individualised treatment of endometrial cancer, improved methods for preoperative tumour characterization are warranted. Texture analysis is a method for quantification of heterogeneity in images, increasingly reported as a promising diagnostic tool in oncological imaging, but largely unexplored in endometrial cancer AIM: To explore whether tumour texture features from preoperative computed tomography (CT) are related to known prognostic histopathological features and to outcome in endometrial cancer patients. Preoperative pelvic contrast-enhanced CT was performed in 155 patients with histologically confirmed endometrial cancer. Tumour ROIs were manually drawn on the section displaying the largest cross-sectional tumour area, using dedicated texture analysis software. Using the filtration-histogram technique, the following texture features were calculated: mean, standard deviation, entropy, mean of positive pixels (MPP), skewness, and kurtosis. These imaging markers were evaluated as predictors of histopathological high-risk features and recurrence- and progression-free survival using multivariable logistic regression and Cox regression analysis, including models adjusting for high-risk status based on preoperative biopsy, magnetic resonance imaging (MRI) findings, and age. High tumour entropy independently predicted deep myometrial invasion (odds ratio [OR] 3.7, p=0.008) and cervical stroma invasion (OR 3.9, p=0.02). High value of MPP (MPP5 >24.2) independently predicted high-risk histological subtype (OR 3.7, p=0.01). Furthermore, high tumour kurtosis tended to independently predict reduced recurrence- and progression-free survival (HR 1.1, p=0.06). CT texture analysis yields promising imaging markers in endometrial cancer and may supplement other imaging techniques in providing a more refined preoperative risk assessment that may ultimately enable better tailored treatment strategies.

Evaluation of adjuvant chemotherapy after abdominal trachelectomy for cervical cancer: a single-institution experience.

To avoid the loss of fertility, chemotherapy should be chosen as an adjuvant treatment after trachelectomy. Our study evaluated the effectiveness and safety of adjuvant chemotherapy after abdominal trachelectomy for cervical cancer. Our institutional review board approved this clinical study, and informed consent was obtained from each patient. We began performing abdominal trachelectomy at our institution in 2005. Deep stromal invasion (more than two-thirds) with lymphovascular space invasion, diffuse cervical invasion, skip lesions in the vagina, and lymphovascular space invasion in the cardinal ligament and vagina were defined as intermediate-risk factors, and parametrial invasion and pelvic lymph node metastasis were defined as high-risk factors. Patients who had intermediate- or high-risk factors received post-trachelectomy adjuvant treatment. The medical records and information of the patients were reviewed retrospectively. Through January 2020, we performed 212 trachelectomies. Among the included patients, 16 and 7 patients with intermediate- and high-risk cancer, respectively, received adjuvant chemotherapy after trachelectomy (2 and 21 patients underwent abdominal modified radical trachelectomy and radical trachelectomy, respectively). Among these patients, only one (4.3%) experienced relapse and subsequent death of the disease after a median postoperative follow-up of 80months (range 12-146months). The 5-year survival rate was 95.5%. Chemotherapy-related life-threatening acute adverse events were not observed. Persistent ovarian dysfunction and late adverse events did not occur. One woman achieved three pregnancies, and two infants were delivered. Adjuvant chemotherapy after abdominal trachelectomy could be an alternative treatment option from the aspects of effectiveness, safety, and fertility preservation.

MiR-4454 up-regulated by HPV16 E6/E7 promotes invasion and migration by targeting ABHD2/NUDT21 in cervical cancer.

The abnormal expression of HPV16 E6/E7 activates oncogenes and/or inactivates tumor suppressor genes, resulting in the selective growth and malignant transformation of cancer cells. miR-4454 was selected by sequencing due to its abnormal high expression in HPV16 E6/E7 positive CaSki cell compared with HPV16 E6/E7 negative C33A cell. Overexpression of miR-4454 enhances cervical cancer cell invasion and migration. ABHD2 and NUDT21 are identified as a target gene of miR-4454.The effects of ABHD2 and NUDT21 on migration and invasion of CaSki and C33A cells were determined. The dual luciferase and RT-qPCR assays confirmed that miR-4454 might regulate its targets ABHD2 and NUDT21 to promote the proliferation, invasion and migration, whereas, inhibit the apoptosis in CaSki and C33A cells.

Long noncoding RNA LUCAT1 promotes cervical cancer cell proliferation and invasion by upregulating MTA1.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Long noncoding RNA LUCAT1 promotes cervical cancer cell proliferation and invasion by upregulating MTA1, by A.-H. Wang, J.-M. Zhao, J. Du, Q.-X. Pang, M.-Q. Wang, published in Eur Rev Med Pharmacol Sci 2019; 23 (16): 6824-6829-DOI: 10.26355/eurrev_201908_18721-PMID: 31486481" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/18721.

Circ_0084927 Facilitates Cervical Cancer Development via Sponging miR-142-3p and Upregulating ARL2.

BackgroundCervical cancer is a fatal burden for women. Circular RNAs (circRNAs) are important regulators in cancer development. Our study aimed to investigate the function and action mechanism of a novel circRNA, circ_0084927, in cervical cancer.MethodsThe expression of circ_0084927, miR-142-3p and ADP-ribosylation factor-like protein 2 (ARL2) mRNA was measured by quantitative real-time polymerase chain reaction (qRT-PCR). For functional analyses, cell proliferation was assessed using cell counting kit-8 (CCK-8) assay. Cell cycle distribution was monitored by flow cytometry assay. Cell migration and cell invasion were evaluated by transwell assay. The interaction between miR-142-3p and circ_0084927 or ARL2 was predicted by the bioinformatics analysis and validated by dual-luciferase reporter assay and RNA immunoprecipitation assay (RIP) assay. The expression of ARL2 at the protein level was detected by Western blot. Animal tumor formation assay was performed to monitor the tumorigenicity of circ_0084927 in vivo.ResultsThe expression of circ_0084927 and ARL2 was enhanced in cervical cancer tissues and cells, while the expression of miR-142-3p was opposite to them. Circ_0084927 knockdown significantly blocked cervical cancer cell proliferation, migration and invasion and induced cell cycle arrest. MiR-142-3p was targeted by circ_0084927, and miR-142-3p inhibition reversed the effects of circ_0084927 knockdown. Besides, miR-142-3p bound to ARL2, and the inhibitory effects of miR-142-3p restoration on cell proliferation, cycle, migration and invasion were counteracted by ARL2 overexpression. More importantly, circ_0084927 upregulated ARL2 expression by sponging miR-142-3p. Circ_0084927 knockdown retarded tumor growth in vivo by regulating miR-142-3p and ARL2.ConclusionCirc_0084927 accelerated the progression of cervical cancer partly by mediating the miR-142-3p/ARL2 axis.

Correlation between heparanase gene polymorphism and susceptibility to endometrial cancer.

BackgroundEndometrial cancer is one of the three most common malignancies in the female genital tract. Previous studies have demonstrated the association between heparanase (HPSE, OMIM 604,724) single‐nucleotide polymorphism (SNP) and cancer risk in several cancers. However, its role in endometrial cancer remains unclear. The present study investigated the effects of HPSE SNPs on the susceptibility and clinicopathological parameters in patients with endometrial cancer.Methods HPSE SNPs of rs4693608 (G > A) and rs4364254 (C > T) were analyzed using polymerase chain reaction‐restriction fragment length polymorphism (PCR‐RFLP) assay in 270 endometrial cancer patients and 320 healthy controls.ResultsThe investigation indicated that the HPSE SNP rs4693608 with GG showed a protective effect from EC in both codominant (adjusted OR = 0.41, 95%CI = 0.21–0.81, p = .026) and recessive models (adjusted OR = 0.43, 95%CI = 0.22–0.82, p = .0076). No significant differences were found in the incidences of EC patients with the rs4364254 polymorphisms compared to controls. Moreover, a significantly increased distribution of A/A (rs4693608) was observed in patients with grade ≥ 2 (p = .03) and in patients with positive cervical invasion (p = .042) while patients with T/C (rs4364254) had lower tumor grade.ConclusionOur study suggested that HPSE SNP of rs4693608 correlated strongly with susceptibility to EC, and HPSE SNPs might be a potential biomarker for prognosis of endometrial cancer.

Long non-coding RNA UCA1 upregulates KIF20A expression to promote cell proliferation and invasion via sponging miR-204 in cervical cancer

ABSTRACT Cervical cancer is a female cancer with the second highest motility over the world. It is urgent to find new therapeutic methods based on long-coding RNAs and microRNAs. UCA1 was proved to be related with many human cancer types, but limited researches have been performed for the inner associations between UCA1 and cervical cancer. Eighty females who were undergoing surgeries were recruited for study in our research. We took the cervical cancer tissues and cells from them. Massive experiments and analysis were conducted to investigate the gene expressions and protein expressions about UCA1, KIF20A, and miR-204 in normal cells and cancer cells. The techniques contain real-time PCR, migration/invasion assay, western blot, in vivo experiments, and so on.We found that UCA1 expression was greatly up-regulated in cervical cancer tissues and cell lines. Our in vitro assays revealed that the suppressing of UCA1 could reduce cervical cancer cells proliferation, migration, and invasion. In addition, we found that lncRNA UCA1 could sponge miR-204 and promote the proliferation and invasion of cervical cancer cells via the up-regulating of KIF20A expression. As a result, the inhibiting of UCA1 could lower cervical cancer (CC) cells growth rate in vivo.Our results identified that UCA1 could serve as an oncogene in cervical cancer cell progression through the modulating of miR-204/KIF20A axis. It gives novel insights to the searching of novel therapeutic methods for cervical cancer.

Prognostic Assessment of Cervical Cancer Patients by Clinical Staging and Surgical-Pathological Factor: A Support Vector Machine-Based Approach.

Introduction: The International Federation of Gynecology and Obstetrics (FIGO) staging system is considered the most powerful prognostic factor in patients with cervical cancer. In addition, other surgical-pathological risk factors have been demonstrated to have significance in predicting the prognosis of patients. Therefore, the purpose of this study was to investigate the effects of the FIGO staging system and surgical-pathological risk factors on the prognosis of cervical cancer patients.Methods: A retrospective study was performed on patients diagnosed with cervical cancer at FIGO stage IB1–IIA2. Kaplan–Meier, Cox proportional hazards regression analysis and the support vector machine (SVM) algorithm were used to assess and validate the high-risk factors related to recurrence and death.Results: A total of 647 patients were included. Kaplan-Meier analysis showed that five high-risk factors, including FIGO stage, status of pelvic lymph node, parametrial involvement, tumor size, and depth of cervical cancer, had a significant effect on the prognosis of patients. In multivariate analysis, pelvic lymph node metastasis (hazard ratio [HR] 2.415, 95% confidence interval [CI] 1.471–3.965), parametrial involvement (HR 2.740, 95% CI 1.092–6.872) and >2/3 depth of cervical invasion (HR 2.263, 95% CI 1.045–4.902) were three independent risk factors of disease-free survival. Pelvic lymph node metastasis (HR 3.855, 95% CI 2.125–6.991) and parametrial involvement (HR 3.871, 95% CI 1.375–10.900) were two independent risk factors for overall survival. When all five high-risk factors were assembled and used for classification prediction through SVM, it achieved the highest prediction accuracy of recurrence (accuracy = 69.1%). The highest prediction accuracy for survival was 94.3% when only using the two independent predictors (the pathological status of lymph nodes and parametrium involvement) by SVM classifiers. Among the 13 groups of intermediate-risk factor, the combination of tumor size, histology and grade of differentiation was more accurate in predicting prognosis than the intermediate-risk factors in the Sedlis criteria (recurrence: 86.8% vs. 60.0%; death: 92.0% vs. 71.6%).Conclusions: The combination of FIGO stage and surgical-pathological risk factors can further enhance the prediction accuracy of the prognosis in patients with early-stage cervical cancer. Histology and grade of differentiation can further improve the prediction accuracy of intermediate-risk factors in the Sedlis criteria.

Predicting Recurrence in Endometrial Cancer Based on a Combination of Classical Parameters and Immunohistochemical Markers.

ObjectiveThe aim of this study was to establish a nomogram to predict the recurrence of endometrial cancer (EC) by immunohistochemical markers and clinicopathological parameters and to evaluate the discriminative power of this model.MethodsThe data of 473 patients with stages I–III endometrial cancer who had received primary surgical treatment between October 2013 and May 2018 were randomly split into two sets: a training cohort and a validation cohort at a predefined ratio of 7:3. Univariate and multivariate Cox regression analysis of screening prognostic factors were performed in the training cohort (n=332) to develop a nomogram model for EC-recurrence prediction, which was further evaluated in the validation cohort (n=141).ResultsUnivariate analysis found that FIGO stage, histological type, histological grade, myometrial invasion, cervical stromal invasion, postoperative adjuvant treatment, and four immunohistochemical markers (Ki67, ER, PR, and p53) were associated with recurrence in EC. Multivariate analysis showed that FIGO stage, histological type, ER, and p53 were superior parameters to generate the nomogram model for recurrence prediction in EC. Recurrence-free survival was better predicted by the proposed nomogram, with a C-index value of 0.79 (95% CI 0.66–0.92) in the validation cohort.ConclusionThis nomogram model involving immunohistochemical markers can better predict recurrence in FIGO stages I–III EC.

A synchronous papillary and follicular thyroid carcinoma presenting as a large toxic nodule in a female adolescent

Case presentationWe report for the first time a synchronous papillary and follicular thyroid carcinoma in a 12-year-old girl presenting with a large (5 cm diameter) left thyroid nodule, an increased left and right upper pole technetium tracer uptake at scintigraphy and hyperthyroidism. The uptake at the right lobe was explained by the crossing of the left nodule to the right site of the neck at Computed Tomography (CT) scanning.BackgroundAlthough thyroid nodules are less common in children than in adults, there is more vigilance required in children because of the higher risk of malignancy. According to literature, about 5% of the thyroid nodules in adults are malignant versus 20–26% in children. The characteristics of 9 other pediatric cases with a differentiated thyroid carcinoma presenting with a toxic nodule, which have been reported during the last 20 years, are summarized. A nodular size of more than 3.5 cm and female predominance was a common finding.ConclusionsThe presence of hyperthyroidism in association with a hyperfunctioning thyroid nodule does not rule out thyroid cancer and warrants careful evaluation, even in the absence of cervical lymph node invasion.

CircRNA circ_POLA2 Promotes Cervical Squamous Cell Carcinoma Progression via Regulating miR-326/GNB1.

Circular RNAs (circRNAs) are a group of non-coding RNAs that have an essential function in the development and progression of various cancers. The expression pattern and function of circRNA in cervical squamous cell carcinoma (CESC) are not fully understood. In the present study, we aimed to investigate the expression profiles and regulation mechanism of circRNA circ_POLA2 in CESC. Circ_POLA2 was highly expressed in CESC tissues and positively correlated with poor prognosis in CESC patients. Knockdown of circ_POLA2 using shRNA inhibited cervical cancer cell proliferation, migration, and invasion both in vitro and in vivo. Mechanistically, circ_POLA2 could sponge endogenous microRNA-326 (miR-326) and inhibit its expression. Furthermore, miR-326 negatively regulated G protein subunit beta 1 (GNB1) by targeting its 3′-UTR. Intriguingly, we found that GNB1 was overexpressed and associated with poor prognosis in CESC patients. Overexpression of GNB1 could antagonize the inhibitory effect of miR-326 on cervical cancer cell proliferation, migration, and invasion. In addition, we demonstrated that circ_POLA2/miR-326/GNB1 axis regulated ERK signaling. In conclusion, circ_POLA2 promotes cervical squamous cell carcinoma development and progression via regulating the miR-326/GNB1 axis, which might serve as a novel therapeutic target for CESC patients.

LINC00319 Promotes Cervical Cancer Progression Via Targeting miR-147a/IGF1R Pathway.

Background: Cervical cancer is identified as the fourth most common female malignancy worldwide. Recently, Linc00319 was reported to play an important role in the development and progression of cervical cancer. However, little is known about the molecular mechanism and clinical significance of Linc00319 in the carcinogenesis of cervical cancer. This study aims to reveal the biological function and molecular mechanisms of Linc00319 in cell proliferation, invasion, and migration of cervical cancer. Materials and Methods: In the current study, gene expression levels of Linc00319, miR-147a, and IFG1R were detected by quantitative real-time PCR in clinical tissue samples and cervical cancer cell lines. Protein levels were also determined by western blot assay in cervical cancer cells. CCK-8, transwell, and wound healing assays were used to test the proliferation, invasion, and migration of cervical cancer cell lines in vitro. Target genes were predicted through bioinformatics methods and then verified by gene engineering technology. Results: The authors' results showed that Linc00319 was upregulated in cervical cancer tissues and cell lines, while Linc00319silencing could inhibit cervical cancer cell proliferation, invasion, and migration. Further investigations showed that Linc00319 interacted with miR-147a and inhibited its expression, unregulated IGF1R to induce progression of cervical cancer. Conclusions: Their research indicated that Linc00319 might play an oncogenic role in cervical cancer and regulate the progression of cervical tumor growth by inhibiting the expression of miR-147a and activating IGF1R-related pathway. The findings suggest a novel molecular biomarker and therapeutic target for cervical tumor and may provide a novel therapeutic strategy for preventing the metastasis of cervical cancer.

Positive peritoneal cytology is an independent risk factor in endometrial cancer.

AbstractObjectiveWe aimed to investigate whether positive peritoneal cytology could serve as a prognostic factor in endometrial cancer (EC).MethodsFrom patients with EC surgically treated at Peking University People's Hospital between 2006 and 2016, 520 patients were selected for retrospective investigation. Clinical and pathologic factors associated with positive peritoneal cytology were assessed using univariate and multivariate logistic regressions model. Disease‐free survival (DFS) and overall survival (OS) were evaluated using Kaplan–Meier estimation and multivariate Cox regressions model.Results(i) The incidence of positive peritoneal cytology in EC patients was 9.0% (47/520). (ii) Multivariate analysis showed that the independent risk factors of positive peritoneal cytology were nonendometrioid carcinoma (odds ratio [OR] = 4.0, 95% confidence interval [CI], 1.8–8.8, P = 0.001), tumor diameter ≥2 cm (OR = 3.2, 95% CI, 1.2–8.7, P = 0.023), cervical stromal invasion (OR = 2.9, 95% CI, 1.3–6.6, P = 0.009) and distant metastasis (OR = 6.5, 95% CI, 1.7–25.4, P = 0.007). (iii) The 5‐year DFS and 5‐year OS of the positive peritoneal cytology group were significantly lower compared with the negative group (54.0% vs 93.2%, P < 0.001; 63.6% vs 94.6%, P < 0.001). (iv) After other contributing factors were adjusted in the multivariable model, positive peritoneal cytology remained an independent predictor of decreased DFS (OR = 2.8, 95% CI, 1.3–6.0, P = 0.007) and OS (OR = 2.8, 95% CI, 1.0–7.2, P = 0.035).ConclusionPositive peritoneal cytology was an independent risk factor in EC patients. Even though it is no longer an indicator according to the current International Federation of Gynecology and Obstetrics staging system, the peritoneal cytology status should still be considered for accurate risk stratification in EC.

MiR-204-5p/TFAP2A feedback loop positively regulates the proliferation, migration, invasion and EMT process in cervical cancer.

MicroRNAs (MiRNAs) have been clarified as crucial regulators of the pathological processes in various carcinomas in the past years. Interestingly, existing evidence has manifested that microRNA-204-5p (miR-204-5p) is engaged in the initiation and progression of multiple carcinomas. However, the potential of miR-204-5p in cervical cancer remains to be disentombed. This study focused on unraveling the detailed role of miR-204-5p in cervical cancer. MiR-204-5p exhibited a low level in cervical cancer cells. The functional assays demonstrated that miR-204-5p upregulation exerted suppressive impact on the functions of cervical cancer cells, including proliferation, invasion, migration and epithelial-mesenchymal transition (EMT) process. Moreover, transcription factor AP-2 alpha (TFAP2A) was screened to be the most affected target gene by miR-204-5p, and TFAP2A was discovered to transcriptionally repress miR-204-5p in cervical cancer. The mutual regulation between TFAP2A and miR-204-5p was testified through molecular mechanism assays. Final rescued-function assays demonstrated that overexpression of TFAP2A could recover the suppressed cellular process caused by miR-204-5p upregulation. In conclusion, miR-204-5p/TFAP2A feedback loop promoted the proliferative and motorial capacities of cervical cancer cells. This finding suggested a novel modulatory loop of miR-204-5p/TFAP2A in cervical cancer, offering promising biomarkers for cervical cancer therapy.

Effects of miR-214 on cervical cancer cell proliferation, apoptosis and invasion via modulating PI3K/AKT/mTOR signal pathway.

Since this article has been suspected of research misconduct and the corresponding authors did not respond to our request to prove originality of data and figures, "Effects of miR-214 on cervical cancer cell proliferation, apoptosis and invasion via modulating PI3K/AKT/mTOR signal pathway, by F. Wang, W.-H. Tan, W. Liu, Y.-X. Jin, D.-D. Dong, X.-J. Zhao, Q. Liu, published in Eur Rev Med Pharmacol Sci 2018; 22 (7): 1891-1898-DOI: 10.26355/eurrev_201804_14711-PMID: 29687840" has been withdrawn. The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/14711.

Long Noncoding RNA ST7-AS1 Upregulates TRPM7 Expression by Sponging microRNA-543 to Promote Cervical Cancer Progression.

PurposeST7 antisense RNA 1 (ST7-AS1) is a long noncoding RNA that affects the progression of gastric cancer and laryngeal squamous cell carcinoma. Herein, ST7-AS1 expression was detected in cervical cancer tissues and cell lines. In addition, its biological roles in inducing the aggressive phenotype of cervical cancer and its associated mechanisms of action were illustrated.Patients and MethodsST7-AS1 expression in cervical cancer tissues and cell lines was detected using quantitative real-time polymerase chain reaction (qRT-PCR). Malignancy was determined using Cell Counting Kit-8 assay, flow cytometry, transwell migration and invasion assays, and xenograft experiments. Bioinformatics analysis was performed to predict the interaction between ST7-AS1 and microRNA-543 (miR-543). Luciferase reporter assay, RNA immunoprecipitation assay, Western blotting, qRT-PCR, and rescue experiments were performed to further identify the interactions among ST7-AS1, miR-543, and transient receptor potential melastatin 7 (TRPM7).ResultsST7-AS1 was upregulated in cervical cancer tissues and cell lines. ST7-AS1 overexpression was correlated with a high International Federation of Gynecology and Obstetrics stage, frequent lymph node metastasis, deep cervical invasion, and short overall survival in patients with cervical cancer. ST7-AS1 inhibition hindered cervical cancer cell proliferation, migration, and invasion; ST7-AS1 downregulation resulted in marked cell apoptosis. Additionally, ST7-AS1 deficiency restricted cervical tumor growth in vivo. Mechanistically, ST7-AS1 functioned as competing endogenous RNA to increase TRPM7 expression by sponging miR-543. Intriguingly, rescue experiments revealed that miR-543 downregulation or TRPM7 overexpression abrogated the inhibitory actions of ST7-AS1 knockdown in the aggressive phenotype of cervical cancer cells.ConclusionThe newly identified ST7-AS1/miR-543/TRPM7 axis promoted the oncogenicity of cervical cancer cells both in vitro and in vivo. Our study highlighted the importance of this novel axis in cervical cancer progression, suggesting that this pathway can serve as a promising therapeutic target for cervical cancer.

Molecular Characterization of Second Primary Endometrial Cancer.

The objective of this study was to determine the molecular and clinicopathological features, as well as the prognosis of patients with endometrial cancer (EC) having prior malignancy (second primary EC: SPEC) compared with those without a history of prior malignancy (first primary EC: FPEC). We enrolled 294 FPEC patients and 32 SPEC patients who had undergone surgical resection with curative intent. EC was divided into four groups according to Cancer Genome Atlas Research Network (TCGA) classification. SPEC patients having greater than a 10-year interval from prior malignancy had risk factors including type II histology, deeper myometrial invasion, cervical invasion, and copy number high (CNH) phenotype compared with patients having less than a 10-year interval (p=0.007, p=0.002, p=0.015 and p=0.001). SPEC patients having greater than a 10-year interval from prior malignancy possessed numerous high-risk factors for EC.

CAF-1/p150 promotes cell proliferation, migration, invasion and predicts a poor prognosis in patients with cervical cancer.

Cervical cancer is one of the most common malignancies among women worldwide that exhibits high morbidity and mortality rates. Thus, the discovery of novel molecules and targets for cervical cancer diagnosis and treatment is critical. The present study aimed to investigate the role of the chromatin assembly factor (CAF)-1 subunit, CAF-1/p150 on cervical cancer cell proliferation, migration and invasion. Immunohistochemical analysis was used to detect the CAF-1/p150 expression in cervical cancer tissues and to analyze the association between CAF-1/p150 expression and the prognosis of patients with cervical cancer. In addition, colony formation, wound healing and Transwell assays were used to assess the function of CAF-1/p150 in cervical cancer cells. The results demonstrated that CAF-1/p150 was expressed in both normal and cervical cancer tissues. CAF-1/p150 protein expression was localized in the cell nuclei and was highly expressed in cervical cancer tissues. Furthermore, high CAF-1/p150 expression was significantly associated with FIGO stage, local recurrence, distant metastasis and a shorter overall survival time of patients with cervical cancer. CAF-1/p150 knockdown attenuated the anchorage-independent proliferation, migration and invasion of Hela and SiHa cervical cancer cells in vitro. Taken together, the results of the present study confirmed the involvement of CAF-1/p150 in the progression of cervical cancer, and validated its use as a poor prognostic indicator in patients with cervical cancer.

Curcumin inhibits cervical cancer cell proliferation, migration and invasion by suppressing the PI3K/AKT signaling pathway via the miR-29b/KDM2A axis

Curcumin inhibits cervical cancer cell proliferation, migration and invasion by suppressing the PI3K/AKT signaling pathway via the miR-29b/KDM2A axis

MicroRNA-362-3p Inhibits Migration and Invasion via Targeting BCAP31 in Cervical Cancer.

Cervical cancer (CC) is the most common malignant tumor in gynecology, and metastasis is an important cause of patient death. MiRNAs (microRNAs) have been found to play key roles in cervical cancer metastasis, but the effect of miR-362-3p in CC is unclear. This study aimed to investigate the role of miR-362-3p in cervical cancer migration and invasion. We compared the expression levels of miR-362-3p in cervical cancer tissues and adjacent normal cervical tissues. In CC tissues, miR-362-3p expression was significantly down-regulated, which is related to the cancer stage and patient survival. MiR-362-3p can effectively inhibit the migration and invasion of cervical cancer cells. The dual-luciferase reporter assay results showed that BCAP31 (B cell receptor associated protein 31) is a direct target protein of miR-362-3p. The results of the immunohistochemical examination of clinical tissue samples showed that BCAP31 was abnormally highly expressed in cervical cancer, which was positively correlated with the clinical stage. BCAP31 knockdown exerted similar effects as miR-362-3p overexpression. Further GSEA analysis showed that BCAP31 may participate in multiple biological processes, such as protein transport, metabolism, and organelle organization. Our results suggest that miR-362-3p inhibits migration and invasion via directly targeting BCAP31 in cervical cancer, and restoring miR-362-3p levels may be a new treatment strategy for cervical cancer in the future.