Proteomic profiling of tumor-initiating cells in HT-29 human colorectal cancer cells

Lee, Han Na; Park, Soo Hyun; Lee, Eun Kyung; Raymundo, Bernardo; Kim, Chan Wha

doi:10.1016/j.bbrc.2012.09.036

Cited by 11 publications

(7 citation statements)

References 42 publications

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“…CD133 and SOX2 expression levels in CD133(+) cells were at least 16-fold and 3-fold higher than those in CD133 (−) cells, respectively (p < 0.001). As previously reported, 10) profilin 2 was significantly up-regulated in CD133(+) cells and its expression level was at least 3-fold higher than that in CD133(−) cells (p < 0.001) ( Fig. 1(B)).…”

Section: Ht29 Cd133(+) Cells Possess Stemness Properties and Metastatsupporting

confidence: 85%

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Profilin 2 promotes migration, invasion, and stemness of HT29 human colorectal cancer stem cells

Kim

Lee

Han

et al. 2015

Bioscience, Biotechnology, and Biochemistry

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We investigated the role of profilin 2 in the stemness, migration, and invasion of HT29 cancer stem cells (CSCs). Increased and decreased levels of profilin 2 significantly enhanced and suppressed the self-renewal, migration, and invasion ability of HT29 CSCs, respectively. Moreover, profilin 2 directly regulated the expression of stemness markers (CD133, SOX2, and β-catenin) and epithelial mesenchymal transition (EMT) markers (E-cadherin and snail). CD133 and β-catenin were up-regulated by overexpression of profilin 2 and down-regulated by depletion of profilin 2. SOX2 was decreased by profilin 2 depletion. E-cadherin was not influenced by profilin 2-overexpression but increased by profilin 2-knockdown. The expression of snail was suppressed by profilin 2-knockdown. We speculated that stemness and the EMT are closely linked through profilin 2-related pathways. Therefore, this study indicates that profilin 2 affects the metastatic potential and stemness of colorectal CSCs by regulating EMT-and stemness-related proteins.

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Section: Ht29 Cd133(+) Cells Possess Stemness Properties and Metastatsupporting

confidence: 85%

“…8,9) Profilin 2 was recently reported to be up-regulated in colorectal CSCs. 10) Profilin is a ubiquitous 15 kDa actin-binding protein found in eukaryotes. In humans, profilin 1 11) and profilin 2 cDNA sequences have been isolated.…”

Section: Introductionmentioning

confidence: 99%

Profilin 2 promotes migration, invasion, and stemness of HT29 human colorectal cancer stem cells

Kim

Lee

Han

et al. 2015

Bioscience, Biotechnology, and Biochemistry

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“…For instance, one research showed that PFN2 mRNA levels and protein were significantly up-regulated in lung cancer tissues, whilst PFN2 overexpression strongly promoted lung cancer migration and invasion [ 19 ]. Another study reported that up-regulated PFN2 expression in colorectal cancer stem cells enhanced the ability of migration and invasion [ 34 , 43 ]. By contrast, Ma et al observed a decreased PFN2 protein expression in OSCC tissues and suggested that the down-expression of PFN2 in OSCC tissues was significantly associated with vascular invasion and advanced TNM stage [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

PFN2, a novel marker of unfavorable prognosis, is a potential therapeutic target involved in esophageal squamous cell carcinoma

Cui

Zhang

et al. 2016

J Transl Med

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BackgroundEsophageal squamous cell carcinoma (ESCC) is one of the most aggressively malignant tumors with dismal prognosis. Profilin 2 (PFN2) is an actin-binding protein that regulates the dynamics of actin polymerization and plays a key role in cell motility. Recently, PFN2 have emerged as significant regulators of cancer processes. However, the clinical significance and biological function of PFN2 in ESCC remain unclear.MethodsPFN2 protein expression was validated by immunohistochemistry (IHC) on tissue microarray from Chinese Han and Kazakh populations with ESCC. The associations among PFN2 expression, clinicopathological features, and prognosis of ESCC were analyzed. The effects on cell proliferation, invasion and migration were examined using MTT and Transwell assays. Markers of epithelial–mesenchymal transition (EMT) were detected by Western blot analysis.ResultsCompared with normal esophageal epithelium (NEE), PFN2 protein expression was markedly increased in low-grade intraepithelial neoplasia (LGIN), high-grade intraepithelial neoplasia (HGIN), and ESCC, increased gradually from LGIN to ESCC, and finally reached high grade in HGIN in the Han population. Similarly, PFN2 protein was more overexpressed in ESCC than in NEE in the Kazakh population. The results of Western blot analysis also showed that PFN2 expression was significantly higher in the ESCC tissue than in a matched adjacent non-cancerous tissue. PFN2 expression was positively correlated with invasion depth and lymph node metastasis. High PFN2 expression was significantly correlated with short overall survival (OS) (P = 0.023). Cox regression analysis revealed that PFN2 expression was an independent prognostic factor for poor OS in ESCC. Downregulation of PFN2 inhibited, rather than proliferated, cell invasion and migration, as well as induced an EMT phenotype, including increased expression of epithelial marker E-cadherin, decreased mesenchymal marker Vimentin, Snail, Slug and ZEB1, and morphological changes in ESCC cells in vitro.ConclusionsOur findings demonstrate that PFN2 has a novel role in promoting ESCC progression and metastasis and portending a poor prognosis, indicating that PFN2 could act as an early biomarker of high-risk population. Targeting PFN2 may offer a promising therapeutic strategy for ESCC treatment.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-016-0884-y) contains supplementary material, which is available to authorized users.

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“…An increase has been seen in colorectal cancer 29 , 30 and in a head and neck cancer cell line (FaDu DD ), under hypoxia, 31 but a decrease in FBA has been recorded in squamous cell carcinoma 32 and in HT-29 cells expressing the cancer stem cell marker CD133. 33 …”

Section: Discussionmentioning

confidence: 99%

Homogenous and Microbeam X-Ray Radiation Induces Proteomic Changes in the Brains of Irradiated Rats and in the Brains of Nonirradiated Cage Mate Rats

et al. 2018

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To evaluate microbeam radiation therapy (MRT), for brain tumor treatment, the bystander effect in nonirradiated companion animals was investigated. Adult rats were irradiated with 35 or 350 Gy at the European Synchrotron Research Facility using homogenous irradiation (HR) or MRT to the right brain hemisphere. The irradiated rats were housed with nonirradiated rats. After 48 hours, all rats were euthanized and the frontal lobe proteome was analyzed using 2-dimensional electrophoresis and mass spectrometry. Proteome changes were determined by analysis of variance (P < .05). Homogenous irradiation increased serum albumin, heat shock protein 71 (HSP-71), triosephosphate isomerase (TPI), fructose bisphosphate aldolase (FBA), and prohibitin and decreased dihydrolipoyl dehydrogenase (DLD) and pyruvate kinase. Microbeam radiation therapy increased HSP-71, FBA, and prohibitin, and decreased aconitase, dihydropyrimidinase, TPI, tubulin DLD, and pyruvate kinase. Cage mates with HR irradiated rats showed increased HSP-71 and FBA and decreased pyruvate kinase, DLD, and aconitase. Cage mates with MRT irradiated rats showed increased HSP-71, prohibitin, and FBA and decreased aconitase and DLD. Homogenous irradiation proteome changes indicated tumorigenesis, while MRT proteome changes indicated an oxidative stress response. The bystander effect of proteome changes appeared antitumorigenic and inducing radioresistance. This investigation also supports the need for research into prohibitin interaction with HSP-70/71 chaperones and cancer therapy.

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Proteomic profiling of tumor-initiating cells in HT-29 human colorectal cancer cells

Cited by 11 publications

References 42 publications

Profilin 2 promotes migration, invasion, and stemness of HT29 human colorectal cancer stem cells

Profilin 2 promotes migration, invasion, and stemness of HT29 human colorectal cancer stem cells

PFN2, a novel marker of unfavorable prognosis, is a potential therapeutic target involved in esophageal squamous cell carcinoma

Homogenous and Microbeam X-Ray Radiation Induces Proteomic Changes in the Brains of Irradiated Rats and in the Brains of Nonirradiated Cage Mate Rats

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