Primary mucinous tumors of the renal pelvis: Clinical, histopathological, and molecular analysis of three cases.

Primary mucinous tumors of the renal pelvis are extremely rare and pose challenges in terms of diagnosis and treatment. This study reviewed the clinical and pathological characteristics of mucinous tumors of the renal pelvis, including mucinous cystadenocarcinomas and mucinous cystadenomas. Immunohistochemical analysis was conducted in three cases, along with KRAS gene detection using the Amplification Refractory Mutation System (ARMS) method. The results revealed mucinous epithelium with acellular mucinous pools in all cases, and acellular mucinous pools were observed in the renal parenchyma and perirenal fat capsules. All tumors expressed CK20 and CDX2, and one case showed KRAS gene mutation. The study suggests that mucinous cystadenomas of the renal pelvis may exhibit borderline biological behaviors. This study is the first to report a KRAS gene mutation in a mucinous cystadenoma of the renal pelvis, offering valuable insights into the diagnosis and treatment of this rare condition.

Genetic profile of primary mucinous cystadenocarcinoma of the breast-A case report.

Primary mucinous cystadenocarcinoma of the breast is a rare neoplasm with few reports in the literature. Here, we report for the first time a comprehensive genetic profile of a primary mucinous cystadenocarcinoma of the breast, using next-generation sequencing 580 cancer-associated gene panel. Mutations in TP53, RB1, and BAP1 were identified. The findings suggest that this tumor is driven mostly by abnormalities in tumor suppressor genes, primarily involved in cell cycle control and chromatin remodeling. Molecular characterization of additional primary mucinous cystadenocarcinomas of the breast is warranted and might provide information related to its biology and behavior.

Multiple KRAS mutations in the non-mucinous epithelial lining in the majority of mucinous cystic neoplasms of the pancreas.

AIMS: Mucinous cystic neoplasms (MCNs) of the pancreas are cystic neoplasms lined by mucinous lining epithelium (MLE) with associated ovarian-type stroma. Although a non-MLE (NMLE) can be observed in some MCNs, whether cystic neoplasms with ovarian-type stroma and NMLE should be classified as MCNs or separately designated is debated. METHODS AND RESULTS: To test this, NMLEs were defined as flat or cuboidal epithelial cells without intracytoplasmic mucin. A total of 112 MCNs were reviewed, and the epithelium was classified as NMLE or MLE. A total of 110 females and two males with a mean age of 46.5 ± 12.3 years were included in this study. At least focal NMLE was noted in 76.8% (86/112) of MCNs. The mean percentage of the neoplastic epithelium that was NMLE in these 86 cases was 46%. NMLE was predominant (>50%) in 38.4% (43/112) of cases. MCNs with NMLE were smaller (42 ± 21 mm) than those with MLE (60 ± 36 mm, P < 0.001), and all NMLEs had low-grade dysplasia. Twelve MCNs with NMLE or MLE were selected for KRAS mutation analysis with droplet digital polymerase chain reaction after laser capture microdissection. All 12 MCNs showed multiple types of KRAS mutation, which were detected in 92% (11/12) of NMLE foci and 89% (8/9) of MLE foci. Predominant NMLE was common in small MCNs with low-grade dysplasia. CONCLUSIONS: Clonal KRAS mutations were observed in both NMLE and MLE, supporting the hypothesis that MCNs with NMLE should be classified as MCNs.

Expression of c-myc and mutation of the KRAS gene in patients with ovarian mucinous tumors.

We examined the expression of c-myc and mutations in the KRAS gene in ovarian mucinous tumors to explore the pathogenesis of these tumors and the feasibility of targeted gene therapy. Expression of c-myc protein and mutations in the KRAS gene in 24 cases of ovarian mucinous cystadenoma, 46 cases of ovarian borderline mucinous cystadenoma, and 46 cases of ovarian mucinous cystadenocarcinoma were detected using the immunohistochemistry PV-9000 2-step method and polymerase chain reaction-restriction fragment length polymorphism. The positive expression rates of c-myc in ovarian mucinous cystadenoma, borderline mucinous cystadenoma, and cystadenocarcinoma were 0, 39.1, and 65.2%, respectively (P < 0.01), while the mutation rates in KRAS were 0, 39.1 and 13.0%, respectively. The mutation rate of the borderline group was significantly higher, while rates in the other 2 groups were similar (P > 0.05). c-myc was not correlated with clinical stage, pathological grade, or age of patients with ovarian mucinous cystadenocarcinoma or borderline mucinous cystadenoma (P > 0.05), but was correlated with tumor size (P < 0.05). Mutations in KRAS were not correlated with clinical stage or tumor size in patients with borderline mucinous cystadenoma (P > 0.05), whereas it was correlated with age (P < 0.05). In borderline mucinous cystadenoma, c-myc expression and KRAS mutations were not correlated (P > 0.05). c-myc is involved in the formation of ovarian borderline mucinous cystadenoma and mucinous cystadenocarcinoma, and the KRAS gene may contribute to the formation of borderline mucinous cystadenoma.

Primary mucinous cystadenocarcinoma of the breast with amplification of the HER2 gene confirmed by FISH - case report and review of the literature.

Fifty five-years-old woman was presented to the general surgery upon the palpation of a mass in her left breast. In the excisional biopsy performed, partially cystic tumor of 2 × 1 cm with solid areas was macroscopically observed. After through microscopic examination, the patient was diagnosed as invasive mucinous cystadenocarcinoma and the tumor was found to be ER- and PR-negative and C-erbB2 (2+). In the fluorescent in situ hybridization, HER2/neu gene amplification was observed. Here, we present the clinical, cytological, morphological and immunohistochemical features of a very rare type of breast carcinoma, mucinous cystadenocarcinoma of the breast, with the review of the relevant literature.

Molecular abnormalities in ovarian carcinoma: clinical, morphological and therapeutic correlates.

The histopathological classification of ovarian surface epithelial carcinomas (referred to hereafter as 'ovarian carcinoma') has shifted over the past 10 years to reflect more clearly our understanding of molecular events during carcinogenesis. Ovarian carcinoma is no longer viewed as a single entity but as multiple disease processes, with each having different molecular pathways altered during oncogenesis, resulting in differences in clinical and pathological features, such as biomarker expression, pattern of spread and response to chemotherapy. There are five subtypes of ovarian carcinoma that are sufficiently distinct and well-characterized that they should be considered to be different diseases, i.e. high-grade serous, clear cell, endometrioid, mucinous and low-grade serous, from most to least common, respectively. This review summarizes the molecular abnormalities of these five ovarian carcinoma subtypes, relating them to clinical and pathological features.

Molecular pathways in pancreatic carcinogenesis.

Pancreatic cancer is a genetic disease. Pancreatic cancers develop from one of three precursor lesions, pancreatic intraepithelial neoplasia (PanIN), intraductal papillary mucinous neoplasms (IPMNs), and mucinous cystic neoplasms (MCNs), and each arises in association with distinct genetic alterations. These alterations not only provide insight into the fundamental origins of pancreatic cancer but provide ample opportunity for improving early diagnosis and management of cystic precursors.

Analysis of microsatellite instability and loss of heterozygosity in ovarian cancer: a study in the population of Espírito Santo, Brazil.

Ovarian cancer is currently the most lethal gynecological malignancy in women. It is a heterogeneous and cytogenetically complex disease previously associated with genomic instability. Our purpose was to analyze microsatellite markers to determine patterns and levels of instability as well as possible correlations with histopathological parameters. Polymerase chain reaction was used to characterize microsatellite instability (MSI) and loss of heterozygosity (LOH) in 24 ovarian tumors at 12 microsatellite loci. A total of 11 samples displayed MSI or LOH. Only low-level MSI was found. Markers D5S346 and CYP11 showed the highest MSI and LOH frequencies. D17S250 LOH was significantly associated with tumor histological type (P = 0.0003), and estrogen receptor α was also associated with tumor histological type (P = 0.048) when a combined analysis of LOH and MSI was performed. Furthermore, LOH was observed in a greater number of markers compared with those displaying MSI. Thus, our results support that MSI is less common than LOH in ovarian cancers.

Mammary mucinous cystadenocarcinoma with long-term follow-up: molecular information and literature review.

BACKGROUND: Mucinous cystadenocarcinoma (MCA) is a very rare form of breast cancer that was first described in 1998. Only 33 cases of primary MCA, including our present case, have been reported thus far. As a consequence, its molecular features, prognosis and treatment regimen are poorly known. Here, we describe a less common presentation of MCA, detail its molecular features, discuss the major differential diagnosis, and provide a brief review of the literature. CASE PRESENTATION: A 59-year-old woman presented with a breast lump in which mammography showed a well-defined nodule. Core needle biopsy (CNB) revealed several lesions lined by tall columnar cells with stratification and abundant mucinous secretion; excision was recommended for final diagnosis. The resected specimens showed cavities of different sizes without surrounding myoepithelial cells. The cavities were rich in mucus, and the nuclei were located at the base of the cells, containing intracellular mucus. Immunohistochemical analysis revealed that it was triple-negative breast cancer (TNBC). Next-generation sequencing (NGS) revealed pathogenic mutations in the PIK3CA, KRAS, MAP2K4, RB1, KDR, PKHD1, TERT, and TP53 genes. A diagnosis of MCA was rendered. The patient has been followed up for 108 months to date and showed no signs of recurrence or metastasis. CONCLUSION: Our study presents the gene profile of an MCA case with no recurrence or metastatic tendency after 108 months of follow-up, and a review of the literature helps us better understand the clinical, pathologic, and molecular features of this tumor.

A comparative analysis of K-ras mutation and carcinoembryonic antigen in pancreatic cyst fluid.

BACKGROUND/AIMS: Analysis of cystic fluid may be useful in distinguishing between benign and malignant cysts which has significant impact on their management. The aim of our study was to assess the diagnostic utility of carcinoembryonic antigen (CEA) and K-ras gene mutation in pancreatic cysts fluid. METHODS: The study included 56 patients with pancreatic cystic fluid collected for analysis. The cysts were classified as benign (simple cysts, pseudocysts, serous cystadenoma) - 39 patients or premalignant/malignant (mucinous cystadenoma, IPMN, cystadenocarcinoma) - 17 patients. The patients history, CEA fluid concentrations and presence of K-ras mutation were analyzed. RESULTS: CEA were higher in patients with malignant cysts (mean levels 238 ± 12.5 ng/ml; range 32.8-4985 ng/ml) compared to benign lesions (mean levels 34.5 ± 3.7 ng/ml; range 3.9-693 ng/ml; p < 0.001). K-ras mutation correctly classified 11 of 17 patients with premalignant/malignant lesions. It was also detected in 1 patient with final diagnosis of benign cyst (the sensitivity 64.7% and the specificity 97.4%; p < 0.01). If CEA and molecular analysis were combined in that cysts with either CEA level>45 ng/ml or presence of K-ras mutation, than 16 of 17 premalignant/malignant cysts were correctly identified (94.1%). CONCLUSION: Molecular analysis of pancreatic cyst fluid adds diagnostic value to the preoperative diagnosis and should be considered when cyst cytologic examination is negative for malignancy.

LAPTM4B polymorphisms is associated with ovarian cancer susceptibility and its prognosis.

OBJECTIVE: Lysosome-associated protein transmembrane 4 beta (LAPTM4B) is an important novel gene associated with the proliferation and differentiation of cells. Recent studies have shown that it was overexpressed in many cancer tissues. This study investigated the association between different LAPTM4B polymorphisms and the susceptibility and prognosis of ovarian cancer. METHODS: A case-control study was performed in 282 patients with ovarian cancer and 365 control subjects. Genomic DNA was extracted from peripheral blood lymphocytes in all participants. LAPTM4B genotypes were determined using polymerase chain reaction. RESULTS: There was a significantly higher LAPTM4B 2 allele frequency in ovarian cancer cases than controls (P < 0.05). Using the LAPTM4B 1/1 genotype as the reference, we found that the LAPTM4B 1/2 and LAPTM4B 2/2 genotypes were positively associated with ovarian cancer. Additionally, we found a negative correlation between the tumor grade and LAPTM4B allele genotype, which indicates strongly that LAPTM4B 2 could affect the survival of patients. CONCLUSIONS: These findings indicate that the LAPTM4B 2 allele may be a risk factor for ovarian cancer and may play an important role in genetic susceptibility to ovarian cancer.

Silencing of CXCR4 blocks progression of ovarian cancer and depresses canonical Wnt signaling pathway.

OBJECTIVE: CXC chemokine receptor 4 (CXCR4) was considered to be an important factor in cancer cell metastasis. This study was aimed to examine the expression of CXCR4 in ovarian cancer and determine the functions and the possible mechanisms of CXCR4 in the progression of ovarian cancer. METHODS: CXC chemokine receptor 4 messenger RNA expression in normal ovarian tissues, malignant epithelial ovarian tumors, and 3 ovarian cancer cell lines was analyzed. Immunohistochemical analysis was used to detect the protein expression of CXCR4 and ß-catenin in normal and malignant ovarian tissues. The effect of CXCR4 inhibition on cell proliferation and invasion was determined. RESULTS: CXC chemokine receptor 4 was highly expressed in malignant ovarian tumors and ovarian cancer cell lines, and the different expression of CXCR4 was observed between the ovarian cancers with lymph node metastasis and without lymph node metastasis. Furthermore, The CXCR4 expression was correlated with ß-catenin expression in ovarian tissues. Moreover, knockdown of CXCR4 could obviously reduce proliferation and invasion of ovarian cancer cell and inhibit Wnt target genes and mesenchymal markers such as vimentin and SLUG expression. CONCLUSIONS: CXC chemokine receptor 4 plays a critical role in the metastasis of human ovarian cancer possibly through modulating the Wnt/ß-catenin pathway. CXC chemokine receptor 4 is a potential therapeutic target for treatment of ovarian cancer.

A study of the methylation status of opioid binding protein/cell adhesion molecule-like gene in ovarian cancer using nested methylation-specific polymerase chain reaction detection.

BACKGROUND: The goal was to improve the methylation-specific PCR (MSP) method and investigate the methylation status of the OPCML gene in carcinoma tissues from ovarian cancer patients. METHODS: MSP and nested MSP methods were used to examine the methylation status of the OPCML gene promoter in ovarian cancer, borderline tumor, and normal ovary tissues. RESULTS: Methylation of the OPCML gene was detected in 58.3% (14/24) and 83.3% (20/24) of the specimens from ovarian cancer patients using MSP and nested MSP methods, respectively. No methylation was observed in normal ovarian tissues using either method. CONCLUSIONS: The modified nested MSP method showed better sensitivity. The methylation of the OPCML gene was significantly higher in ovarian cancer than in normal tissue. The detection of OPCML gene methylation could serve as one of the molecular markers for the diagnosis of ovarian cancer.

[Expression of hSef and FGF-2 in epithelial ovarian tumor].

OBJECTIVE: To detect the expression of human similar expression to FGF gene(hSef) and fibroblast growth factor-2(FGF-2) and their correlation with epithelial ovarian tumor. METHODS: Immunohistochemical SP staining was used to detect the expression of hSef and FGF-2 proteins in 31 cases of epithelial ovarian carcinoma (EOC), 18 cases of benign epithelial tumor (BET), 10 cases of normal ovarian (NO) tissues collected from July 2007 to May 2008. The expression of hSef mRNA in 24 cases of EOC, BET and NO collected from July 2008 to May 2009 were analyzed by RT-PCR. RESULTS: The results of immunohistochemical study showed that the expression of hSef in the EOC tissues were significantly lower than that in the NO and BET (P < 0.001). However, the expression of FGF-2 was higher (P = 0.002). The expression of hSef had a negative correlation with FGF-2 (r(s) = -0.324, P = 0.012). The RT-PCR results showed that there was a gradually declined trend of expression of hSef in NO, BET to EOC (P < 0.001), but the expression of FGF-2 in NO, BET to EOC was gradually increased (P < 0.001), with a significant negative correlation (NO: r(s) = -0.910, P < 0.001; BET: r(s) = -0.859, P < 0.001; EOC: r(s) = -0.888, P < 0.001). CONCLUSIONS: The expression of hSef is decreased in epithelial ovarian carcinoma tissue, but the expression of FGF-2 is increased. It is likely that low hSef expression is related to the the carcinogenesis and development of epithelial ovarian carcinoma by suppressing the promoting effects of FGF-2 to cell proliferation.

miR­224­5p regulates the proliferation, migration and invasion of pancreatic mucinous cystadenocarcinoma by targeting PTEN.

Pancreatic mucinous cystadenocarcinoma (MCC) is a rare malignant tumor, with a limited number of studies. The present study aimed to investigate the function and mechanism of microRNA (miR)­224­5p on proliferation, migration and invasion of MCC of the pancreas. Reverse transcription­quantitative PCR was used to explorethe expression of miR­224­5p and the PTEN gene. MTT, wound healing, Transwell and tumorigenesis assays were conducted to investigate the proliferation, migration and invasion of MCC1 cells in vitro and in vivo. Western blot analysis was employed to test the protein expression of PTEN. The target gene of miR­224­5p was assessed and verified by luciferase assay. miR­224­5p expression was notably higher, while PTEN expression was lower, in MCC1 cells compared with normal tissues and cells. Overexpression of miR­224­5p promoted the proliferation, migration and invasion of MCC and knockdown of miR­224­5p inhibited these functions. Bioinformatics analysis and luciferase assay indicated that PTEN was the direct target gene of miR­224­5p. The negative correlation between miR­224­5p and PTEN was confirmed both in vitro and in vivo. PTEN reversed the effects of miR­224­5p on proliferation, migration and invasion of MCC1 cells. The present study revealed for the first time, to the best of the authors' knowledge, that miR­224­5p was highly expressed and served an oncogenic role in MCC. miR­224­5p not only regulated the proliferation, migration and invasion of pancreatic MCC but may also be a potential therapeutic target for MCC.

Primary Mucinous Cystadenocarcinoma of the Breast: A Rare Case Report With Review of Literature.

Primary mucinous cystadenocarcinoma (MCA) of the breast is a rare variant of breast carcinoma known to have a favorable prognosis despite showing a basal-like phenotype. We describe a case of MCA breast in a 45-year-old female with a palpable mass in the breast. On the basis of the histopathological and immunohistochemical evaluation of a lumpectomy specimen with the absence of mass anywhere else on whole-body imaging, a diagnosis of primary MCA was rendered. Mismatch repair protein evaluation showed this tumor to be microsatellite stable. Molecular testing revealed the absence of Kirsten rat sarcoma viral oncogene homolog (KRAS), neuroblastoma RAS viral oncogene homolog (NRAS), and v-raf murine sarcoma viral oncogene homolog B1 (BRAF) mutations. To date only 27 cases of MCA breast have been reported. To the best of our knowledge, ours is the first case documenting diffuse Cytokeratin 20 (CK20) positivity, microsatellite stability, and the absence of KRAS, NRAS, and BRAF mutations in these tumors. The rarity of this tumor further evokes an interest in this case. A better understanding of the disease warrants a review of more cases with longer follow-ups.

Association of epidermal growth factor receptor and mitogen-activated protein kinase with cystic neoplasms of the pancreas.

The molecular pathobiology of pancreatic cystic neoplasms is poorly understood. The aim of this study was to know the involvement of epidermal growth factor receptor (EGFR) and its downstream targets in the serous cystic neoplasms and the mucinous cystic neoplasms of the pancreas. In a total of 72 pancreatic cystic neoplasms, including 39 serous cystic neoplasms and 33 mucinous cystic neoplasms, we examined the expression of native and phosphorylated EGFR, mitogen-activated protein kinase (MAPK), and AKT by immunohistochemistry and somatic mutations in EGFR, KRAS, BRAF, and PIK3CA, by direct sequencing. We also assessed the copy numbers of EGFR transcripts and the amplification of the EGFR gene in some of the samples. We found that EGFR, phosphorylated EGFR, MAPK, and phosphorylated MAPK were evidently expressed in 100, 54, 100, and 69% of the serous cystic neoplasms, and in 12%, none, 33, and 27% of the mucinous cystic neoplasms, respectively; the expression was significantly higher and more prevalent in the serous cystic neoplasms than in the mucinous cystic neoplasms. The expression of AKT and phosphorylated AKT was low in both the types of neoplasms. On average, EGFR transcripts in the serous cystic neoplasms and the mucinous cystic neoplasms increased 53.5- and 2.5-fold, respectively, as compared with that in normal tissues, with the increase in the former being significantly greater than that in the latter. Amplification of the EGFR gene was not detected in any of the examined serous cystic neoplasms. None of the tumors had mutations in any of the examined portions of the genes, except two mucinous cystic neoplasms with mutations in codon-12 of KRAS. These results indicate that EGFR and MAPK are actively involved in the pathobiology of serous cystic neoplasms and may therefore be potential diagnostic markers and therapeutic targets in patients with the above mentioned types of neoplasms.

[Expression of EVEC in ovarian carcinoma and its biological significance].

OBJECTIVE: To investigate the expression of EVEC in ovarian carcinoma and explore its biological significance. METHODS: The expression of EVEC in 22 specimens of normal ovarian tissues and 63 specimens of ovarian cancers was detected by RT-PCR and Western blotting analysis, respectively. RESULTS: RT-PCR showed that the expression level of EVEC in stage I-II ovarian cancer (0.199 ± 0.014) was significantly higher than that in stage III-IV ovarian cancer (0.155 ± 0.015, P < 0.05), and significantly lower than that in normal ovarian tissues (0.415 ± 0.055, P < 0.05). There was no significant difference between the expression levels of EVEC in primary sites and that in corresponding metastatic sites of ovarian cancer (P > 0.05). Furthermore, the results of Western blot also showed that the protein expression level of EVEC in stage I-II ovarian cancer was also significantly lower than that in normal ovarian tissues (0.179 ± 0.026 vs. 0.543 ± 0.032, P < 0.05), and higher than that in stage III-IV ovarian cancer (0.179 ± 0.026 vs. 0.115 ± 0.023, P < 0.05). The EVEC expression level in the epiploic metastasis of stage I-II ovarian cancer was significantly higher than that of stage III-IV ovarian cancer (0.201 ± 0.028 vs. 0.101 ± 0.037, P < 0.05). The expression of EVEC in ovarian carcinoma had no correlation with age, pathologic classification and histological grade (P > 0.05). CONCLUSIONS: EVEC is closely related with carcinoma metastasis. The expression of EVEC in ovarian cancer and its metastatic sites was remarkably decreased. EVEC may play a negative role in the development and metastasis of ovarian cancer and may be a valuable marker in estimation of the prognosis for patients.

Ovarian mucinous tumors with mural nodules: immunohistochemical and molecular analysis of 3 cases.

BACKGROUND: Primary ovarian mucinous tumors with mural nodules are very rare. The histogenesis of the mural nodules remains unclear. METHODS: We investigated the clincopathological and molecular features in 3 cases with mural nodules. RESULTS: Patient 1 was diagnosed as mucinous carcinoma with mural nodules of anaplastic carcinoma that was composed of CK+ and CK7+ spindled cells and polygonal cells with marked pleomorphism. Aberrant p53 staining was found in the mural nodules rather than in the mucinous components. A concordant KRAS mutation (c.35G > A p.G12A) was identified in both mucinous tumors and mural nodules. She died of disease at 44 months. The mural nodule in patient 2 was interpreted as a sarcoma, no other specified. The uniform short spindle cells were separated by abundant myxoid matrix. They were CD10 + , CCND1-, SMA-, and negative for break-apart BCOR, PHF1, and JAZF1 FISH assay. The adenocarcinomatous component harbored LOH at D18S51 and FGA loci while the sarcomatous component had LOH at D19S433. She had lung metastasis at 18 months and was alive without evidence of disease for 40 months. Patient 3 harbored multiple mural nodules that were composed of vimentin+, focal CK+, atypical spindle cells. A diagnosis of sarcoma-like mural nodules was rendered. She was alive with no evidence of disease for 13 months. No hotspot mutant AKT1, KRAS, HRAS, and PI3KCA alleles were found in patients 2 and 3. CONCLUSIONS: Mural nodules with anaplastic carcinoma or with true sarcomas may represent the dedifferentiation form of mucinous tumors or collision tumors, respectively. The worrisome histology in sarcoma-like mural nodules necessitates meticulous treatment for these patients.

Vitamin D regulates cell viability, migration and proliferation by suppressing galectin-3 (Gal-3) gene in ovarian cancer cells.

Vitamin D deficiency is identified as a risk factor for the occurrence and recurrence of ovarian cancer. Galectin-3 (Gal-3) participates in many physiological and pathological processes. In present study, serum vitamin D level was detected using chemiluminescence enzyme immunoassay. Gal-3 expression was examined using real-time polymerase chain reaction (PCR), Western blot and immunocytochemistry analysis. SKOV3 cells viability was assessed by the water-soluble tetrazolium salt (WST-1) assay, the migration of SKOV3 cells was detected using transwell assay, and the proliferation of SKOV3 cells was measured by 3H-thymidine incorporation (3H-TdR). Our study demonstrated that vitamin D levels were lower in 40 ovarian cancer patients: vitamin D deficiency is closely related to the pathogenesis of ovarian cancer. Treatment with vitamin D reduced the migration and proliferation of ovarian cancer cells. Gal-3 was overexpressed in ovarian cancer, which could induce the viability, migration and proliferation ability of ovarian cancer cells, and these effects were abrogated by vitamin D downregulating the expression of Gal-3 gene. Therefore, our results support that vitamin D may suppress Gal-3-induced viability, migration and proliferation ability of ovarian cancer cells, which suggests that the use of vitamin D may have beneficial effects in preventing and treating ovarian cancer.