Claudin18.2 expression and its clinicopathological feature in adenocarcinoma from various parts.

AIMS: To clarify claudin18.2 expression and its clinicopathological features in various cancers, especially in lung adenocarcinoma. METHODS: Immunohistochemistry staining and fluorescence in situ hybridisation (FISH) were performed to detect claudin18.2 expression and CLDN18 gene rearrangement in adenocarcinoma from different organs. RESULTS: The results showed that claudin18.2 expression was found in 68% (27 of 40) of lung mucinous adenocarcinoma, 52% (16 of 31) of cholangiocarcinoma, 2% (10 of 423) of colorectal adenocarcinoma tissue microarray, 27% (6 of 22) of colorectal mucinous adenocarcinoma and 30% (3 of 10) of cervical adenocarcinoma, but not in all 39 cases of invasive breast adenocarcinoma by immunohistochemistry staining. There was significantly positive correlation between ratio of claudin18.2-positive carcinoma cells and staining intensity in lung mucinous adenocarcinoma and cholangiocarcinoma. Claudin18.2 expression was much more in female patients than male patients with lung mucinous adenocarcinoma. In addition, cholangiocarcinoma with claudin18.2 expression was more aggressive and had perineural invasion. Intraductal papillary neoplasm of the bile duct and epithelial dysplasia of the adjacent bile in cholangiocarcinoma also showed claudin18.2 expression. All three cases of cervical adenocarcinoma with claudin18.2 expression were moderately differentiated adenocarcinoma including one human papillomavirus (HPV)-associated carcinoma, two non-HPV-associated and gastric-type carcinoma. CLDN18 gene rearrangement was not found in all 22 cases with high claudin18.2 expression by FISH. CONCLUSIONS: Our results suggest claudin18.2 might be a potential biomarker for targeted therapy on lung mucinous adenocarcinoma, cholangiocarcinoma, colorectal mucinous adenocarcinoma and gastric-type cervical adenocarcinoma.

Phase separation of DDX21 promotes colorectal cancer metastasis via MCM5-dependent EMT pathway.

RNA binding proteins (RBPs) contributes to cancer progression, but the underlying mechanism reminds unclear. Here, we find that DDX21, a representative RBP, is highly expressed in colorectal cancer (CRC), which leads to CRC cell migration and invasion in vitro, and CRC to liver metastasis and lung metastasis in vivo. This effect of DDX21 on CRC metastasis is correlated to the activation of Epithelial-mesenchymal transition (EMT) pathway. Moreover, we reveal that DDX21 protein is phase separated in vitro and in CRC cells, which controls CRC metastasis. Phase-separated DDX21 highly binds on MCM5 gene locus, which is markedly reduced when phase separation is disrupted by mutations on its intrinsically disordered region (IDR). The impaired metastatic ability of CRC upon DDX21 loss is restored by ectopic expression of MCM5, indicating MCM5 is a key downstream target of DDX21 for CRC metastasis. Furthermore, co-higher expressions of DDX21 and MCM5 is significantly correlated with poor survival outcomes of stage III and IV CRC patients, indicating the importance of this mechanism in CRC late and metastatic stage. Altogether, our results elucidate a new model of DDX21 in regulating CRC metastasis via phase separation.

A clinicopathologic study of 13 cases of primary lymphoma in soft tissue and review of literature.

Primary lymphoma in soft tissue is very rare. In order to understand the clinicopathological features of primary lymphoma in soft tissue, we found 13 cases (0.3%) of primary lymphoma in soft tissue by reviewing 4303 lymphomas diagnosed in our institution from 2010 to 2019. Tumors were found in the following sites: 8 in lower extremity (2 in leg, 1 in calf, 1 in knee and 4 in buttock), 1 in upper extremity (left shoulder) and 4 in the trunk (3 in waist and 1 in thoracolumbar). The most common histologic type was DLBCL (7/13, 54.8%). 6 cases of which had follow-up information. 25 patients were also selected by screening the English literature search (from Jan 2010 to December 2019) including 1102 studies. Compared to the results of literature review, our results are similar with them. The tumor sites were as follows: 10 in lower extremity, 4 in upper extremity, 9 in the trunk and 2 in masticatory muscle. The most common histological type was also DLBCL (n=11/25, 44%). Overall survival analysis of all 31 patients including our 6 cases with primary lymphoma in soft tissue showed no significant difference between different histological type (Log Rank P=0.120, Breslow P=0.157). The differential diagnosis includes malignant melanoma, rhabdomyosarcoma and metastatic carcinoma in soft tissue.

The value of combined PET/MRI, CT and clinical metabolic parameters in differentiating lung adenocarcinoma from squamous cell carcinoma.

Objective: This study aimed to study the diagnostic efficacy of positron emission tomography (PET)/magnetic resonance imaging (MRI), computed tomography (CT) and clinical metabolic parameters in predicting the histological classification of lung adenocarcinoma (ADC) and squamous cell carcinoma (SCC). Methods: PET/MRI, CT and clinical metabolic data of 80 patients with lung ADC or SCC were retrospectively collected. According to the pathological results from surgery or fiberscopy, the patients were diagnosed with lung ADC (47 cases) or SCC (33 cases). All 80 patients were divided into a training group (64 cases), an internal testing group (8 cases) and an external testing group (8 cases) in the ratio of 8:1:1. Nine models were constructed by integrating features from different modalities. The Gaussian classifier was used to differentiate ADC and SCC. The prediction ability was evaluated using the receiver operating characteristic curve. The area under the curve (AUC) of the models was compared using Delong's test. Based on the best composite model, a nomogram was established and evaluated with a calibration curve, decision curve and clinical impact curve. Results: The composite model (PET/MRI + CT + Clinical) owned the highest AUC values in the training, internal testing and external testing sets, respectively. In the training set, significant differences in the AUC were found between the composite model and other models except for the PET/MRI + CT model. The calibration curves showed good consistency between the predicted output and actual disease. The decision curve analysis and clinical impact curves demonstrated that the composite model increased the clinical net benefit for predicting lung cancer subtypes. Conclusion: The composite prediction model of PET/MRI + CT + Clinical better distinguished ADC from SCC pathological subtypes preoperatively and achieved clinical benefits, thus providing an accurate clinical diagnosis.

A diagnosis model in nasopharyngeal carcinoma based on PET/MRI radiomics and semiquantitative parameters.

BACKGROUND: The staging of nasopharyngeal carcinoma (NPC) is of great value in treatment and prognosis. We explored whether a positron emission tomography/ magnetic resonance imaging (PET/MRI) based comprehensive model of radiomics features and semiquantitative parameters was useful for clinical evaluation of NPC staging. MATERIALS AND METHODS: A total of 100 NPC patients diagnosed with non-keratinized undifferentiated carcinoma were divided into early-stage group (I-II) and advanced-stage group (III-IV) and divided into the training set (n = 70) and the testing set (n = 30). Radiomics features (n = 396 × 2) of the primary site of NPC were extracted from MRI and PET images, respectively. Three major semiquantitative parameters of primary sites including maximum standardized uptake value (SUVmax), metabolic tumor volume (MTV), and total lesion glycolysis (TLG) in all NPC patients were measured. After feature selection, three diagnostic models including the radiomics model, the metabolic parameter model, and the combined model were established using logistic regression model. Finally, internal validation was performed, and a nomogram for NPC comprehensive diagnosis has been made. RESULTS: The radiomics model and metabolic parameter model showed an area under the curve (AUC) of 0.83 and 0.80 in the testing set, respectively. The combined model based on radiomics and semiquantitative parameters showed an AUC of 0.90 in the testing set, with the best performance among the three models. CONCLUSION: The combined model based on PET/MRI radiomics and semiquantitative parameters is of great value in the evaluation of clinical stage (early-stage group and advanced-stage group) of NPC.

Clinicopathologic and molecular features of vascular tumors in a series of 118 cases.

AIMS: Vascular tumors are composed of benign, intermediate, and malignant lesions. The diagnosis is challenging because some entities demonstrate overlapping morphologies and harbor the same genetic alterations. We describe herein a cohort of vascular tumors with clinicopathologic, immunohistochemical, and molecular features. METHODS AND RESULTS: 118 vascular tumors including 56 angiosarcomas, 18 epithelioid haemangioendotheliomas (EHE), 25 epithelioid haemangiomas (EH), 8 pseudomyogenic haemangioendotheliomas (PHE), 1 papillary intralymphatic angioendothelioma (PILA), 2 kaposiform haemangioendotheliomas (KHE), 3 Kaposi sarcomas, 2 retiform haemangioendotheliomas (RHE), and 3 anastomosing haemangiomas were assessed. FOSB, c-Fos, CAMTA1, and TFE3 expression and gene rearrangements were analyzed by immunohistochemical staining and FISH, respectively. Our results showed that FOSB expression was diffusely positive in all 8 PHEs, focally or sparsely in 12 EHs, and in 2 angiosarcomas. C-FOS expression was sparsely to diffusely positive in 15 EHs, focally or sparsely in 17 angiosarcomas, 1 EHE, 1 Kaposi sarcoma, and 1 PHE. CAMTA1 expression was positive in only 12 EHEs. TFE3 expression was focally or sparsely positive in all 8 PHEs, 22 angiosarcomas, 6 EHEs, 3 EHs, 2 Kaposi sarcomas, and 2 AHs. FOSB rearrangement was found in 5 PHEs, FOS rearrangement only in 1 EH, CAMTA1 rearrangement in 4 EHEs. CONCLUSIONS: FOSB and CAMTA1 are useful diagnostic markers for PHE and EHE, respectively. FOSB and FOS fusion represent a subset of epithelioid haemangioma. TFE3 is not a diagnostically meaningful marker in a majority of vascular tumors. The combined utility of these markers will facilitate the differential diagnosis in vascular tumors with morphologic overlap.

Positron Emission Tomography/Magnetic Resonance Imaging Radiomics in Predicting Lung Adenocarcinoma and Squamous Cell Carcinoma.

OBJECTIVE: To investigate the diagnostic value of positron emission tomography (PET)/magnetic resonance imaging (MRI) radiomics in predicting the histological classification of lung adenocarcinoma and lung squamous cell carcinoma. METHODS: PET/MRI radiomics and clinical data were retrospectively collected from 61 patients with lung cancer. According to the pathological results of surgery or fiberscope, patients were divided into two groups, lung adenocarcinoma and squamous cell carcinoma group, which were set as positive for adenocarcinoma (40 cases) and negative for squamous cell carcinoma (21 cases). The radiomics characteristics most related to lung cancer classification were calculated and selected using radiomics software, and the two lung cancer groups were randomly assigned into a training set (70%) and a test set (30%). Maximum relevance and minimum redundancy (mRMR) and least absolute shrinkage and selection operator (LASSO) methods in the uAI Research Portal software (United Imaging Intelligence, China) were used to select the desired characteristics from 2600 features extracted from MRI and PET. Eight optimal features were finally retained through 5-fold cross-validation, and a PET/MRI fusion model was constructed. The predictive ability of this model was evaluated by the difference in area under the curve (AUC) obtained from the receiver operating characteristic (ROC) curve. RESULTS: AUC of PET/MRI model for the training group and test group were 0.886 (0.787-0.985) and 0.847 (0.648-1.000), respectively. PET/MRI radiomics features revealed different degrees of correlation with the classification of lung adenocarcinoma and squamous cell carcinoma, with significant differences. CONCLUSION: The prediction model constructed based on PET/MRI radiomics features can predict the preoperative histological classification of lung adenocarcinoma and squamous cell carcinoma without seminality and repeatability. It can also provide an objective basis for accurate clinical diagnosis and individualized treatment, thus having important guiding significance for clinical treatment.

Pan-cancer analysis of oncogenic role of Programmed Cell Death 2 Like (PDCD2L) and validation in colorectal cancer.

BACKGROUND: Programmed Cell Death 2 Like (PDCD2L) correlates with cell proliferation, apoptosis and mouse embryonic development. However, the role of PDCD2L in human cancers is unclear. METHODS: Multiple bioinformatic methods, in vitro function experiments and validation were performed to clarify the oncogenic role of PDCD2L in human cancers. RESULTS: Our study found that PDCD2L was aberrantly expressed in multiple types of human cancers, and associated with clinical stage and molecular subtype. Furthermore, overexpression of PDCD2L predicted poor overall survival in adrenocortical carcinoma(ACC), kidney chromophobe(KICH), acute myeloid leukemia(LAML), brain lower grade glioma(LGG),liver hepatocellular carcinoma(LIHC), mesothelioma(MESO), uveal melanoma(UVM) and poor diseases free survival in ACC, bladder urothelial carcinoma(BLCA), cervical squamous cell carcinoma and endocervical adenocarcinoma (CESC), kidney renal clear cell carcinoma(KIRC), kidney renal papillary cell carcinoma(KIRP), LGG, LIHC, and UVM. PDCD2L expression was negatively associated with cancer associated fibroblast in breast invasive carcinoma (BRCA), lung squamous cell carcinoma (LUSC), sarcoma (SARC), stomach adenocarcinoma (STAD) and testicular germ cell tumors (TGCT). Mechanically, we found that PDCD2L expression was associated with apoptosis, invasion and cell cycle by investigating single cell sequencing data. For further validation, PDCD2Lwas highly expressed in colorectal cancer (CRC) cell lines and tissue samples compared with the normal colon cell line and non-tumor adjacent colorectal mucosa tissues. PDCD2L knockdown induced the apoptosis and proliferation of CRC cells. CONCLUSIONS: Our study shows that the oncogenic role of PDCD2L in various cancers and PDCD2L could be served as a biomarker of CRC.

A Prognosis Marker SLC2A3 Correlates With EMT and Immune Signature in Colorectal Cancer.

SLC2A3 is a membrane transporter that belongs to the solute carrier family, whose function includes transmembrane transport and glucose transmembrane transport activity. To clarify the expression and role of SLC2A3 in colorectal cancer (CRC), we analyzed the TCGA and GEO databases and found that SLC2A3 mRNA levels were significantly higher in CRC tissues than that in adjacent non-tumor tissues. Furthermore, high expression of SLC2A3 predicted poor overall survival and disease free survival for CRC patients. For validation, we collected 174 CRC samples and found that SLC2A3 expression was higher in CRC tissues than that in adjacent non-tumor colorectal mucosa tissues by immunohistochemistry staining. Further study showed that high expression of SLC2A3 was enriched in epithelial-mesenchymal transition (EMT) classical pathway, interferon-γ pathway by GSEA analysis enrichment, indicating that SLC2A3 may play a key role in the progression of CRC through EMT and immune response, which also has been validated by the global gene expression profiling of human CRC cell lines. The expression of SLC2A3 was positively correlated with CD4 and CD8+T cells by using TIMER and EPIC algorithm, respectively. SLC2A3 knockdown suppressed migration and inhibited the expression of Vimentin and MMP9 in CRC cell line SW480 and RKO. Meanwhile, PD-L1 expression was also significantly attenuated in SW480 and RKO cells transfected with SLC2A3 siRNA. The result suggests that SLC2A3 may be involved in the immune response of CRC by regulating PD-L1 immune checkpoint. In our series, SLC2A3 and PD-L1 positive expression was 74% (128/174) and 22% (39/174) of CRC, respectively. SLC2A3 expression was significantly associated with perineural invasion in CRC patients. In conclusion, SLC2A3 may play an important role in progression of CRC by regulating EMT and PD-L1 mediated immune responses.

Radiomics Analysis and Correlation With Metabolic Parameters in Nasopharyngeal Carcinoma Based on PET/MR Imaging.

Objective: Accurate staging is of great importance in treatment selection for patients with nasopharyngeal carcinoma (NPC). The aims of this study were to construct radiomic models of NPC staging based on positron emission tomography (PET) and magnetic resonance (MR) images and to investigate the correlation between metabolic parameters and radiomic features. Methods: A total of 100 consecutive cases of NPC (70 in training and 30 in the testing cohort) with undifferentiated carcinoma confirmed pathologically were recruited. Metabolic parameters of the local lesions of NPC were measured. A total of 396 radiomic features based on PET and MRI images were calculated [including histogram, Haralick, shape factor, gray level co-occurrence matrix (GLCM), and run length matrix (RLM)] and selected [using maximum relevance and minimum redundancy (mRMR) and least shrinkage and selection operator (LASSO)], respectively. The logistic regression models were established according to these features. Finally, the relationship between the metabolic parameters and radiomic features was analyzed. Results: We selected the nine most relevant radiomic features (six from MR images and three from PET images) from local NPC lesions. In the PET model, the area under the receiver operating characteristic (ROC) curve (AUC), accuracy, sensitivity, and the specificity of the training group were 0.84, 0.75, 0.90, and 0.69, respectively. In the MR model, those metrics were 0.85, 0.83, 0.75, and 0.86, respectively. Pearson's correlation analysis showed that the metabolic parameters had different degrees of correlation with the selected radiomic features. Conclusion: The PET and MR radiomic models were helpful in the diagnosis of NPC staging. There were correlations between the metabolic parameters and radiomic features of primary NPC based on PET/MR. In the future, PET/MR-based radiomic models, with further improvement and validation, can be a more useful and economical tool for predicting local invasion and distant metastasis of NPC.

Hemangioblastoma: clinicopathologic study of 42 cases with emphasis on TFE3 expression.

Hemangioblastomas (HBs) histologically overlap with TFE3 rearrangement-associated tumors, which present as alveolar architecture and clear or eosinophilic granular cytoplasm. However, whether TFE3 is expressed in HBs remains unexplored. Herein, we analyzed the clinicopathologic features of 42 HBs emphasizing studies of TFE3 expression. Of 42 cases, 38 were sporadic and 4 were regarded as a part of von Hippel-Lindau (VHL) syndrome according to clinical presentation. Nineteen patients were male and 23 were female. Patient age ranged from 17 to 70 years (median 43). Tumor size ranged from 0.4 to 4.8 cm (mean 2.2 cm). Follow-up ranged from 1 to 60 months and 6 patients developed recurrence. Immunohistochemistry staining showed that 36 (86%) of 42 HBs expressed TFE3 in nuclei of tumor cells, of which 21 were evaluated as high TFE3 expression levels. Increased TFE3 expression was significantly associated with older ages (P=0.018) and larger tumor size (P=0.001). Seventeen HBs with high TFE3 expression were negative for rearrangement and amplification of TFE3 by FISH analysis, 3 of which including 2 sporadic and 1 VHL-related HBs demonstrated trisomies or tetrasomies of X-chromosome in 7%~18% of tumor cells. All 3 cases occurred in female, presented with a larger tumor size and displayed a similar morphologic appearance with high cellularity and hyperchromatic nuclei. Our study first reports TFE3 expression and its clinicopathological relevance in HBs. We hypothesize that TFE3 might be involved in the pathogenesis of non-VHL-related HBs. Furthermore, HBs with strong TFE3 expression should be differentiated from brain-metastatic TFE3-rearranged tumors.

miR-203a-3p promotes colorectal cancer proliferation and migration by targeting PDE4D.

Colorectal cancer (CRC) is a major worldwide health problem due to its high prevalence and mortality rate. microRNA has been reported playing an important role in a variety of cancers including colorectal cancer. miR-203a-3p has been found up-regulated in CRC tissues compare with the adjacent normal tissues. But, how miR-203a-3p regulates CRC development remains to be elucidated. In this study, gain and loss-of-function assays showed that miR-203a-3p promotes colorectal cancer cell proliferation, colony formation and migration and invasion by targeting PDE4D. And miR-203a-3p/ß-catenin/Cyclin D1/c-Myc signaling pathway is involved in the CRC. In summary, this study highlights an onco-miRNA role for miR-203a-3p by regulating PDE4D in CRC and suggests that miR-203a-3p may be a novel molecular therapeutic target for CRC.

GALNT6 suppresses progression of colorectal cancer.

Colorectal cancer (CRC) is one of the most common malignant tumors in the world. Invasion and metastasis are the main cause of mortality in most CRC patients. Polypeptide N-acetylgalactosaminyltransferase 6 (GALNT6) regulated glycosylation, which is frequently altered in cancers, and play an important role in cancer development. However, the role of GALNT6 in CRC remains unknown. To investigate the role of GALNT6 in CRC, first we studied correlation of GALNT6 expression levels with outcomes of CRC patients and found CRC patients with higher expression of GALNT6 had a better overall survival than those with lower expression. In addition, GALNT6 expression were significantly associated with tumor size, histological differentiation and lymph node metastasis. In vitro, GALNT6 overexpression dramatically inhibited cellular colony formation, migration, and invasion, and promoted the apoptosis of CRC cells. In vivo, CRC with GALNT6 overexpression showed reduced pulmonary metastasis in recipient mice compared with the controls. GALNT6 expression was significantly increased in SW480 and SW1116 cells cultured in hypoxic condition, and decreased in HT29 and LOVO cells with oxidative stress. Affimetrix microarray analysis showed that GALNT6 overexpression induced 279 genes up-regulated and 215 genes down-regulated in CRC. GALNT6 overexpression dramatically suppressed AKT and activated CD28 signaling pathway in CRC. AKT rescue experiment found that AKT was involved in GALNT6-induced CRC cell migration and invasion. In conclusion, our results first suggest that GALNT6 plays an important role in development and progression of CRC as a tumor suppressor gene.

miR-338-3p suppresses colorectal cancer proliferation and progression by inhibiting MACC1.

Colorectal cancer (CRC) is one of the most common malignancies worldwide. This study aimed to elucidate the clinicopathological significance of miR-338-3p and its association with metastasis-associated in colon cancer-1 (MACC1) in CRC. We evaluated miR-338-3p and MACC1 expression in CRC cell lines and analyzed the clinicopathological features of miR-338-3p in 98 samples of CRC tissues. Subsequent Western blot and cellular biological techniques, and xenograft mouse models were performed to investigate the biological role of miR-338-3p and its association with MACC1 in CRC. Our results show that miR-338-3p expression is lower in CRC cell lines and tissues than that in a human normal colonic epithelial cell line and adjacent normal colorectal tissue, respectively. miR-338-3p expression was significantly associated with histological differentiation, UICC stage, T classification, N classification, and M classification in 98 samples of CRC. The overall survival of CRC patients was significantly less in the low miR-338-3p expression group than in the high miR-338-3p expression group (p<0.01). miR-338-3p mimics suppressed cell proliferation, colony formation, migration, and invasion, but induced apoptosis in CRC cells. miR-338-3p inhibitor reversed these biological phenotypes. miR-338-3p mimics or inhibitor suppressed or increased MACC1 expression in HCT116 and SW620. miR-338-3p mimics reversed the effect of increased MACC1 expression induced by HCT116 with MACC1 over-expression plasmid. Increased cell proliferation, colony formation, and suppressed cell apoptosis caused by MACC1 over-expression were significantly reversed in HCT116 transfected with miR-338-3p mimics, respectively. Suppressed cell proliferation, colony formation, migration, invasion, and increased cell apoptosis caused by MACC1 knockdown were significantly reversed in SW620 transfected with miR-338-3p inhibitor, respectively. In vivo, miR-338-3p agomir significantly inhibited xenograft CRC tumor growth and reversed the effect of increased xenograft tumor growth induced from HCT116 with MACC1 overexpression. In conclusion, our data suggest that miR-338-3p suppresses CRC carcinogenesis and progression by inhibiting MACC1. Targeting miR-338-3p might be a novel treatment strategy for CRC.

The clinicopathological significance of ZNF10 in invasive ductal carcinoma of the breast.

The aim of this study was to clarify the clinicopathological features and role of zinc finger protein 10 (ZNF10) in breast invasive ductal cancer (IDC). Our data first showed that ZNF10 expression was higher in 8 pairs of fresh breast IDC and breast cancer cell lines compared with their respective adjacent non-tumor breast tissues. ZNF10 expression was significantly higher in IDC compared with DCIS and fibroadenoma of the breast. ZNF10 expression was significantly associated with patients' age, tumor stage, and breast cancer molecular subtype. ZNF10 knockdown inhibited breast cancer cell proliferation, colony formation, cell cycle progression, cell migration, and invasion but induced apoptosis. ZNF10 knockdown also suppressed the tumorigenicity of breast cancer in vivo. The underlying mechanism study showed that ZNF10 regulated the ß-catenin signaling pathway in breast cancer. ZNF10 might bind to the region (nucleotides -300 to +100) of the ß-catenin promoter. In conclusion, our results first suggest that ZNF10 promotes the carcinogenesis and progression of breast IDC via the ß-catenin signaling pathway. Targeting ZNF10 might be a novel treatment strategy for breast cancer.

miR-27a-3p targeting RXRα promotes colorectal cancer progression by activating Wnt/ß-catenin pathway.

This study aimed to elucidate how miR-27a-3p modulates the Wnt/ß-catenin signaling pathway to promote colorectal cancer (CRC) progression. Our results showed that the expression of miR-27a-3p was up-regulated in CRC and closely associated with histological differentiation, clinical stage, distant metastasis and CRC patients' survival. miR-27a-3p mimic suppressed apoptosis and promoted proliferation, migration, invasion of CRC cells in vitro and in vivo. Whereas miR-27a-3p inhibitor promoted apoptosis and suppressed proliferation, migration, invasion of CRC cells in vitro and in vivo. Furthermore, RXRα was the target gene of miR-27a-3p in CRC. miR-27a-3p expression negatively correlated with RXRα expression in CRC tissues. The underlining mechanism study showed that miR-27a-3p/RXRα/Wnt/ß-catenin signaling pathway is involved in CRC progression. In conclusion, our findings first demonstrate that miR-27a-3p is a prognostic and/or potential therapeutic biomarker for CRC patients and RXRα as miR-27a-3p targeting gene plays an important role in activation of the Wnt/ß-catenin pathway during CRC progression.