The Impact of Cysteine-Rich Intestinal Protein 1 (CRIP1) on Thyroid Carcinoma

Abstract

Background/Aims: CRIP1 (cysteine-rich intestinal protein 1) has been found in several tumor types; however, its prognostic impact and role in cellular processes, particularly in thyroid carcinoma, are still unclear. Methods: To elucidate the prognostic impact of CRIP1, we analyzed tissues from 58 primary invasive thyroid carcinomas using immunohistochemistry. Western blotting was performed to investigate CRIP1 protein expression in the thyrocyte cell line Nthy-ori 3-1 and four different thyroid carcinoma cell lines, K1, TPC-1, TT, and SW579. Endogenous expression of CRIP1 was suppressed using a siRNA (si-CRIP1). The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was used to investigate cell viability. Flow cytometric analysis was used to detect cell cycle progression and cell apoptosis. The effects of silencing CRIP1 on cell migration and invasion were detected using the transwell assay. Results: The immunohistochemistry results showed that CRIP1 was overexpressed in thyroid carcinoma. CRIP1 expression was associated with tumor size, TNM stage, and lymphatic metastasis, but not with age, gender, and tumor location. In addition, the expression of CRIP1 in K1, TPC-1, TT, and SW529 cells was higher than that in the Nthy-ori 3-1 cells. The highest expression was observed in the SW579 and TT cells. Furthermore, silencing CRIP1 inhibited the proliferation, migration, and invasion of thyroid carcinoma cell lines SW579 and TT. We also found that silencing CRIP1 induced G1 arrest and apoptosis of thyroid carcinoma cell lines SW579 and TT. Conclusion: In conclusion, CRIP1 acts as an oncogene in the cell proliferation, migration, and invasion processes of thyroid carcinoma. CRIP1 may serve well as an independent prognostic marker with significant predictive power for use in thyroid carcinoma therapy.

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

“…Thus, it may function as an oncogene to regulate the migration and invasion of CRC cells and may be regarded as a new promising biomarker for poor prognosis and the metastasis of colon cancer. Similar results were also found in cervical cancer [ 17 ], thyroid carcinoma [ 18 ], and endometrial cancer [ 19 ]. In contrast, CRIP1 expression led to a favourable outcome and fewer metastases in osteosarcoma [ 20 ] and breast cancer [ 21 ].…”

Cysteine-rich intestinal protein 1 suppresses apoptosis and chemosensitivity to 5-fluorouracil in colorectal cancer through ubiquitin-mediated Fas degradation

“…CRIP1 was further detected in immune cells in tissues of rats, suggested the involvement of this protein in host defense [6]. Aberrant expression of CRIP1 was also mentioned in several tumor types including prostate cancer, pancreatic caner, cervical cancer, breast cancer, osteosarcoma, gastric cancer, and thyroid cancer [7–13]. However, related studies are very limited and the role of CRIP1 is controversial in different tumor types.…”

Terminal web and vesicle trafficking proteins mediate nematode single-cell tubulogenesis

“…Journal of Cell Biology 2 of 15 Nematode terminal web mediates tubulogenesis https://doi.org/10.1083/jcb.202003152 act in a genetic pathway to regulate canal morphology: EXC-9/ CRIP1, EXC-1/IRG, and EXC-5/FGD (Grussendorf et al, 2016;Mattingly and Buechner, 2011;Tong and Buechner, 2008). All of the three encoded proteins have close human homologues: CRIP1 increases metastatic transformation and invasiveness in cell culture (Cousins and Lanningham-Foster, 2000;He et al, 2017;Li et al, 2017;Zhang et al, 2018); IRGM is involved with autophagy and pathogenic responses (Howard et al, 2011;Kumar et al, 2018;Pilla-Moffett et al, 2016); and FGD genes are loci of the developmental diseases Aarskog-Scott syndrome and Charcot-Marie-Tooth disease type 4H (Delague et al, 2007;Gao et al, 2001;Stendel et al, 2007). Mutants in these nematode genes show similar cystic defects in the structure of the canal apical surface as well as defects in vesicle transport: buildup of RAB-5-labeled vesicles and loss of RME-1-labeled vesicles in areas of cystic dilation (Grussendorf et al, 2016;Mattingly and Buechner, 2011).…”