Knockdown of CSE1L Gene in Colorectal Cancer Reduces Tumorigenesis in Vitro

Pimiento, José M.; Neill, Kevin G; Henderson-Jackson, Evita; Eschrich, Steven; Chen, Dung Tsa; Husain, Kazim; Shibata, David; Coppola, Domenico; Malafa, Mokenge P.

doi:10.1016/j.ajpath.2016.06.016

Cited by 25 publications

(41 citation statements)

References 26 publications

(32 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Previous studies have found that CSE1L knockdown resulted in decreased cell proliferation, a reduction in colony formation in soft agar, and induction of apoptosis in colorectal cancer30. Yuksel et al 31.…”

Section: Discussionmentioning

confidence: 99%

CSE1L interaction with MSH6 promotes osteosarcoma progression and predicts poor patient survival

Cheng

Lin

et al. 2017

Sci Rep

View full text Add to dashboard Cite

To discover tumor-associated proteins in osteosarcoma, a quantitative proteomic analysis was performed to identify proteins that were differentially expressed between osteosarcoma and human osteoblastic cells. Through clinical screening and a functional evaluation, chromosome segregation 1-like (CSE1L) protein was found to be related to the growth of osteosarcoma cells. To date, little is known about the function and underlying mechanism of CSE1L in osteosarcoma. In the present study, we show that knockdown of CSE1L inhibits osteosarcoma growth in vitro and in vivo. By co-immunoprecipitation and RNA-seq analysis, CSE1L was found to interact with mutS homolog 6 (MSH6) and function as a positive regulator of MSH6 protein in osteosarcoma cells. A rescue study showed that decreased growth of osteosarcoma cells by CSE1L knockdown was reversed by MSH6 overexpression, indicating that the activity of CSE1L was an MSH6-dependent function. In addition, depletion of MSH6 hindered cellular proliferation in vitro and in vivo. Notably, CSE1L expression was correlated with MSH6 expression in tumor samples and was associated with poor prognosis in patients with osteosarcoma. Taken together, our results demonstrate that the CSE1L-MSH6 axis has an important role in osteosarcoma progression.

show abstract

Section: Discussionmentioning

confidence: 99%

CSE1L interaction with MSH6 promotes osteosarcoma progression and predicts poor patient survival

Cheng

Lin

et al. 2017

Sci Rep

View full text Add to dashboard Cite

show abstract

“…44 Pimiento reported that CSE1L knockdown inhibited cell proliferation and induced apoptosis in CRC cells. 45 Li found that CSE1L acted as an oncogene in gastric cancer (GC), and knockdown of CSE1L suppressed GC cell proliferation and metastasis via inhibition of glycoprotein nonmetastatic melanoma protein B (GPNMB) expression. 46 In this study, analysis of GEO datasets (GSE110224 and GSE37364) and IHC analysis showed that CSE1L was upregulated in CRC.…”

Section: Discussionmentioning

confidence: 99%

<p>Circular RNA 0060745, a Novel circRNA, Promotes Colorectal Cancer Cell Proliferation and Metastasis Through miR-4736 Sponging</p>

Wang

Ren

et al. 2020

OTT

View full text Add to dashboard Cite

Purpose: Recent studies have shown that noncoding RNAs (ncRNAs) play essential roles in the development of a number of cancers. Circular RNAs (circRNAs) have been shown to contribute to the progression of colorectal cancer (CRC). Methods: In this study, the expression levels of circular RNA 0060745 (circ_0060745), and microRNA 4736 (miR-4736) were measured using qRT-PCR. Kaplan-Meier survival analysis and receiver operating characteristic (ROC) analysis were used to evaluate the diagnostic value of circ_0060745. Transwell assay and cell counting kit-8 (CCK8) assay were used to determine the metastatic and proliferative capacity of CRC cells. The expression of chromosome segregation one like (CSE1L) was measured using Western blotting and immunohistochemistry (IHC). In addition, RNA pull-down assay and luciferase assay were performed to verify the targeted binding between miR-473,6 and circ_0060745, and between as miR-4736 and CSE1L. Results: We showed that circ_0060745 was upregulated in CRC, and was associated with unfavorable clinicopathological characteristics. We also showed that circ_0060745 acted as an oncogene and promoted CRC cell proliferation and metastasis. Circ_0060745 was primarily located in the cytoplasm. Furthermore, miR-4736 was downregulated in CRC, was a downstream target of circ_0060745, and mediated proliferation and metastasis. We showed that circ_0060745 sequestered miR-4736, which resulted in CRC cell proliferation and metastasis. Finally, we showed that CSE1L, a downstream target of miR-4736, was upregulated in CRC and mediated suppression of proliferation and metastasis in CRC. Conclusion: The results of this study showed that circ_0060745 promoted CRC cell proliferation and metastasis via modulation of miR-4736/CSE1L signaling. The Circ_0060745/miR-4736/CSE1L axis might be a novel target for the treatment of CRC.

show abstract

“…Also, CSE1L expression was increased in ovarian cancer, and the depletion of CSE1L impaired invasion and metastasis of ovarian cancer cells [ 32 ]. Moreover, as mentioned above, CSE1L was reported to be closely linked with the occurrence and progression CRC [ 14 – 16 ].…”

Section: Discussionmentioning

confidence: 99%

“…CSE1L, highly expressed in various cancer types, plays important roles in apoptosis, cell survival, chromosome assembly, nucleocytoplasmic transport, microvesicle formation, and cancer metastasis [ 12 , 13 ]. In CRC, CSE1L expression was upregulated and CSE1L knockdown suppressed cell proliferation, metastasis, and induced apoptosis [ 14 – 16 ]. However, whether the effect of CSE1L on CRC pathogenesis was mediated by BANCR is still obscure.…”

Section: Introductionmentioning

confidence: 99%

LncRNA BANCR promotes tumorigenesis and enhances adriamycin resistance in colorectal cancer

Yang

Liu

et al. 2018

Aging

View full text Add to dashboard Cite

Colorectal cancer (CRC) is the third most common malignancy in the United States. Chemotherapeutic resistance is a massive obstacle for cancer treatment. The roles and molecular basis of long non-coding RNA BRAF-activated noncoding RNA (BANCR) in CRC progression and adriamycin (ADR) resistance have not been extensively identified. In this study, we found that BANCR and CSE1L expressions were upregulated in CRC tumor tissues. Meanwhile, CSE1L expression was correlated with depth of CRC. BANCR silencing suppressed cell proliferation and invasion capacity, increased apoptotic rate and potentiated cell sensitivity to ADR. CSE1L downregulation triggered a reduction of cell proliferation and invasion ability, and an increase of apoptosis rate and cell sensitivity to ADR. CSE1L overexpression attenuated si-BANCR-mediated anti-proliferation, anti-invasion and pro-apoptosis effects in CRC cells. BANCR acted as a molecular sponge of miR-203 to sequester miR-203 away from CSE1L in CRC cells, resulting in the upregulation of CSE1L expression. CSE1L knockdown inhibited expressions of DNA-repair-related proteins (53BP1 and FEN1) in HCT116 cells. BANCR knockdown also inhibited tumor growth and enhanced ADR sensitivity in CRC mice model. In conclusion, BANCR knockdown suppressed CRC progression and strengthened chemosensitization of CRC cells to ADR possibly by regulating miR-203/CSE1L axis, indicating that BANCR might be a promising target for CRC treatment.

show abstract

Knockdown of CSE1L Gene in Colorectal Cancer Reduces Tumorigenesis in Vitro

Cited by 25 publications

References 26 publications

CSE1L interaction with MSH6 promotes osteosarcoma progression and predicts poor patient survival

CSE1L interaction with MSH6 promotes osteosarcoma progression and predicts poor patient survival

<p>Circular RNA 0060745, a Novel circRNA, Promotes Colorectal Cancer Cell Proliferation and Metastasis Through miR-4736 Sponging</p>

LncRNA BANCR promotes tumorigenesis and enhances adriamycin resistance in colorectal cancer

Contact Info

Product

Resources

About