CRIP1 promotes cell migration, invasion and epithelial-mesenchymal transition of cervical cancer by activating the Wnt/β‑catenin signaling pathway.

Cervical cancer (CC) is the third most common cancer and the fourth leading cause of malignancy-related mortality in women worldwide. In addition, epithelial-mesenchymal transition (EMT) has been generally studied in tumor metastasis researches in recent years. Cysteine-rich intestinal protein 1 (CRIP1) is differently expressed in human cancer cells. However, the role it plays in CC has not been revealed at present. Preliminary experiments have shown that CRIP1 had a higher expression in CC tissues, compared with adjacent noncancerous tissues. Real-time PCR and western blot were performed to analyze CRIP1 expression in CC cell lines. CRIP1 transient transfection vector and siRNA were constructed. Further analysis revealed the promotion effects of CRIP1 on the cell migration and invasion of CC in vitro (P < 0.01). In addition, western blot was performed to show that CRIP1 mediates EMT by means of EMT marker detection. The expression of CRIP1 and β‑catenin in CC tissues was analyzed by immunohistochemistry (IHC). Interestingly, CRIP1 and β‑catenin were both highly expressed in CC tissues (P < 0.01). Furthermore, CRIP1 increased the protein expression level of c-myc, cyclinD-1 and cytoplasmic β‑catenin, which are indicators for activating the Wnt/β‑catenin signaling pathway. In conclusion, CRIP1 promotes cell migration and invasion, mediates EMT and activates the Wnt/β‑catenin signaling pathway in CC.

Zhang LZ ，Huang LY ，Huang AL ，Liu JX ，Yang F ... -  《-》

Cysteine-Rich Intestinal Protein 1 Served as an Epithelial Ovarian Cancer Marker via Promoting Wnt/β-Catenin-Mediated EMT and Tumour Metastasis.

To explore the expression, functions, and the possible mechanisms of cysteine-rich intestinal protein 1 (CRIP1) in epithelial ovarian cancer. Using open microarray datasets from The Cancer Genome Atlas (TCGA), we identified the tumorigenic genes in ovarian cancer. Then, we detected CRIP1 expression in 26 pairs of epithelial ovarian cancer tissue samples by immunohistochemistry (IHC) and performed a correlation analysis between CRIP1 and the clinicopathological features. In addition, epithelial ovarian cancer cell lines A2780 and OVCAR3 were used to examine CRIP1 expression by western blot and qRT-PCR. Various cell function experiments related to tumorigenesis were performed including the CCK8 assay, EdU, Annexin V-FITC/PI apoptosis assay, wound healing, and Transwell assay. In addition, the expression of epithelial-mesenchymal transition (EMT) markers was detected by western blot to illustrate the relationship between CRIP1 and EMT. Furthermore, KEGG pathway enrichment analysis and western blot were conducted to reveal the signaling pathways in which CRIP1 is involved in ovarian cancer pathogenesis. CRIP1 was identified as an oncogene from the TCGA database. The IHC score demonstrated that the CRIP1 protein was expressed at a higher level in tumours than in tumour-adjacent tissues and was associated with a higher pathological stage, grade, and positive lymphatic metastasis. In cell models, CRIP1 was overexpressed in serous epithelial ovarian cancer. Cell function experiments showed that the knockdown of CRIP1 did not significantly affect cell proliferation or apoptosis but could exert an inhibitory effect on cell migration and invasion, and also induce changes in EMT markers. Furthermore, KEGG pathway enrichment analysis and western blot showed that CRIP1 could induce ovarian cancer cell metastasis through activation of the Wnt/β-catenin pathway. This study is the first to demonstrate that CRIP1 acts as an oncogene and may promote tumour metastasis by regulating the EMT-related Wnt/β-catenin signaling pathway, suggesting that CRIP1 may be an important biomarker for ovarian cancer metastasis and progression.

Liu Y ，Li W ，Luo J ，Wu Y ，Xu Y ，Chen T ，Zhang W ，Fu F ... -  《-》

Golgi Phosphoprotein 3 Promotes Cervical Cancer Progression via Wnt/β-catenin Mediated Epithelial-Mesenchymal Transition.

Cervical cancer (CC) is one of the fatal malignancies affecting the life expectancy of women worldwide. Golgi Phosphoprotein 3 (GOLPH3) has been shown to play a key role in the development of various tumors. However, the role of GOLPH3 in the development of CC is unclear. GOLPH3 levels were measured using quantitative real-time polymerase chain reaction (qRT-PCR) and western blot assays. Cell Counting Kit-8 (CCK-8) and colony formation assays were used to detect cell proliferation. Xenograft tumor models were used to explore the effects of GOLPH3 on tumor growth of mice, and immunohistochemistry assay was performed to determine the expression of GOLPH3 and Ki-67. Transwell assay was performed to evaluate cell migration and invasion. Western blot assay was used to analyze the signaling molecules-related proteins regulated by GOLPH3. GOLPH3 was upregulated in human CC tissues from the GEO database (GSE39001 and GSE63514), and further demonstrated that GOLPH3 level was elevated in human CC cells. GOLPH3 enhanced CC cell proliferation, and knockdown of GOLPH3 suppressed tumor growth and decreased Ki-67 level in xenograft mice. In addition, GOLPH3 aggravated the migration and invasion of CC cells. The data indicated that Wnt/β-catenin signaling might be one of the key targets of GOLPH3. Blockage of the Wnt/β-catenin pathway by XAV-939 significantly affected the effects of GOLPH3 on cell proliferation and epithelial-mesenchymal transition (EMT) related molecules, whereas LiCl (a Wnt/β-catenin signal activator) reversed these above effects. GOLPH3 promotes cell proliferation, migration and invasion in CC, possibly by regulating the Wnt/β-catenin signaling pathway, which may provide a new idea for the development of CC therapeutic targets.

Yang H ，Ma X ，Song B ，Wang D ，Chai Z ... -  《-》

Astragalus polysaccharide inhibits breast cancer cell migration and invasion by regulating epithelial‑mesenchymal transition via the Wnt/β‑catenin signaling pathway.

Yang S ，Sun S ，Xu W ，Yu B ，Wang G ，Wang H ... -  《-》

SNHG3/WISP2 Axis Promotes Hela Cell Migration and Invasion via Activating Wnt/β-Catenin Signaling.

Xu D ，Feng H ，Ren Z ，Li X ，Jiang C ，Chen Y ，Liu L ，Chen W ，Cui Z ，Cang S ... -  《-》