Expression of CAS/CSE1L, the Cellular Apoptosis Susceptibility Protein, Correlates With Neoplastic Progression in Barrett’s Esophagus

Jiang, Kun; Neill, Kevin G; Cowden, Daniel; Klapman, Jason; Eschrich, Steven A.; Pimiento, José M.; Malafa, Mokenge P.; Coppola, Domenico

doi:10.1097/pai.0000000000000464

Cited by 8 publications

(7 citation statements)

References 22 publications

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“…The relation between CSE1L and digestive tract tumors have been reported previously in a many research (Ayham et al, 2012;Jiang et al, 2016;Liao et al, 2008). The expression of CES1L was closely associated with pathological stages, tissue types, and neoplastic progression (Ayham et al, 2012).…”

Section: Discussionsupporting

confidence: 61%

CSE1L silence inhibits the growth and metastasis in gastric cancer by repressing GPNMB via positively regulating transcription factor MITF

Yuan

Liu

et al. 2019

Journal Cellular Physiology

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Human chromosomal segregation 1-like (CSE1L) gene functions as a key molecular mediator in cellular proliferation, invasion, and apoptosis. The association of CSE1L with tumor progression has been reported in diverse human cancers. A greater understanding of CSE1L molecular mechanism is beneficial for cancer treatment. In the current study, we show that CSE1L was highly expressed in gastric cancer (GC)

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Section: Discussionsupporting

confidence: 61%

CSE1L silence inhibits the growth and metastasis in gastric cancer by repressing GPNMB via positively regulating transcription factor MITF

Yuan

Liu

et al. 2019

Journal Cellular Physiology

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“…CSE1L silencing could induce apoptosis and repress the proliferation and invasion of gastric cancer cells by regulating the PI3K/Akt/mTOR and MEK/ERK signaling pathways ( 18 ). In addition, a recent study revealed that the abnormal expression of CSE1L was correlated with neoplastic progression in Barrett’s esophagus ( 19 ). However, the role of CSE1L has not been studied in esophageal cancer.…”

Section: Discussionmentioning

confidence: 99%

FLVCR1 Predicts Poor Prognosis and Promotes Malignant Phenotype in Esophageal Squamous Cell Carcinoma via Upregulating CSE1L

et al. 2021

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ObjectiveDysregulation of feline leukemia virus subgroup C receptor 1(FLVCR1) expression has been investigated in several tumors. However, the expression and role of FLVCR1 in esophageal squamous cell carcinoma (ESCC) remain largely unknown.MethodsFLVCR1 expression in tissues was measured by immunohistochemical staining (IHC). Celigo assay, MTT assay, colony formation, caspase 3/7 activity analysis, wound healing assay, Transwell migration, and invasion assay were applied to assess the effects of FLVCR1 on ESCC tumorigenesis. Coimmunoprecipitation (Co-IP) and liquid chromatography-mass spectrometry (LC-MS) were used to identify protein interactions with FLVCR1. An in vivo imaging system (IVIS) was used to investigate the functions of FLVCR1 on the growth and metastatic capability of ESCC cells in a xenograft model and a tail vein metastasis model.ResultsElevated expression of FLVCR1 was detected in ESCC tissues and predicted poor survival. Upregulated FLVCR1 was positively correlated with lymph node metastasis (N stage) and late tumor-node-metastasis (TNM) stage. FLVCR1 knockdown inhibited cell proliferation and colony formation ability, induced cell apoptosis, and repressed cell migration and invasion of ESCC in vitro. Inhibition of FLVCR1 markedly repressed tumorigenicity and metastasis of ESCC cells in vivo. Mechanistically, chromosome segregation 1–like (CSE1L) was identified to interact with FLVCR1 using a Co-IP assay. Moreover, the inhibitory effect of FLVCR1 knockdown on proliferation and migration was counteracted by the exogenous expression of CSE1L.ConclusionFLVCR1 plays a pivotal role in ESCC cell survival, growth, and migration. These functions may be partially dependent upon the protein interaction between FLVCR1 and CSE1L. In addition, FLVCR1 can be applied as a clinical prognostic marker for patients with ESCC.

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“…Therefore, we used microRNA target predictions starBase and identified gene targets associated with cell proliferation and apoptosis in NPC. One such predicted target, CSE1L , has been demonstrated to modulate tumor malignancy in various cellular models [ 15 , 18 , 20 , 47 ], and it is highly expressed in NPC cells [ 21 , 22 , 41 ]. However, it is not clear whether interaction between miR-451a and CSE1L accounts for the tumor-suppressive effects observed in NPC.…”

Section: Discussionmentioning

confidence: 99%

The microRNA-451a/chromosome segregation 1-like axis suppresses cell proliferation, migration, and invasion and induces apoptosis in nasopharyngeal carcinoma

Luo

Kan

et al. 2021

Bioengineered

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Expression of CAS/CSE1L, the Cellular Apoptosis Susceptibility Protein, Correlates With Neoplastic Progression in Barrett’s Esophagus

Abstract: These findings show changes in CAS/CSE1L during BE progression. CAS/CSE1L may represent a potential marker for dysplasia/carcinoma.

Cited by 8 publications

References 22 publications

CSE1L silence inhibits the growth and metastasis in gastric cancer by repressing GPNMB via positively regulating transcription factor MITF

CSE1L silence inhibits the growth and metastasis in gastric cancer by repressing GPNMB via positively regulating transcription factor MITF

FLVCR1 Predicts Poor Prognosis and Promotes Malignant Phenotype in Esophageal Squamous Cell Carcinoma via Upregulating CSE1L

The microRNA-451a/chromosome segregation 1-like axis suppresses cell proliferation, migration, and invasion and induces apoptosis in nasopharyngeal carcinoma

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