An overview of esophageal squamous cell carcinoma proteomics

Qi, Yi-Jun; Chao, Wei-Xia; Chiu, Jen‐Fu

doi:10.1016/j.jprot.2012.04.025

Cited by 44 publications

(35 citation statements)

References 51 publications

(88 reference statements)

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“…Recent studies from our laboratory and others have identified more than 200 different cytoskeleton constituents or binding proteins. However, only about 45 kinds have been reported in ESCC [21]. Hence, the 15 biomarkers used here include biomarkers that are reported for the first time.…”

Section: Discussionmentioning

confidence: 99%

A three-protein signature and clinical outcome in esophageal squamous cell carcinoma

et al. 2014

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Current staging is inadequate to precisely predict clinical outcome of esophageal squamous cell carcinoma (ESCC) and determine treatment choices, which vary from operation alone to intensive multimodal regimens. The purpose of this study is to investigate the prognostic values of an immunohistochemistry-based three-protein signature model in patients with ESCC. We determined the protein expression of Annexin II, cofilin 1, ezrin, fascin, kindlin-2, moesin, MTSS1, myosin-9, profilin-1, Rac1, radixin, ROCK2, talin, tensin and villin 1 in a test cohort including 110 formalin-fixed, paraffin-embedded esophageal curative resection specimens by tissue microarrays (TMAs). A three-protein signature elicited from the protein cluster, Annexin II, kindlin-2, and myosin-9, was validated by TMAs on an independent cohort of 147 specimens. The expression of three-protein signature was highly predictive of ESCC overall survival (OS) and disease-free survival (DFS) in both generation and validation datasets. Regression analysis shows that this three-protein signature is an independent predictor for OS and DFS. Furthermore, the predictive ability of these 3 biomarkers in combination is more robust than that of each individual biomarker. This study demonstrates a clinically applicable prognostic model that accurately predicts ESCC patient survival and/or tumor recurrence, and thus could serve as a complement to current risk stratification approaches.

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Section: Discussionmentioning

confidence: 99%

A three-protein signature and clinical outcome in esophageal squamous cell carcinoma

et al. 2014

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“…Proteomic technologies have been used to identify cancer biomarkers and therapeutic targets; especially, 2-diffusion electrophoresis (DE) coupled with mass spectrometry (MS) has been widely applied to analyze protein profiling of ESCC [7] as well as various other cancers including colorectal, hepatocellular, and lung cancer [8]. In our previous study, using MALDI-TOF-MS, five upregulated proteins were identified Electronic supplementary material The online version of this article (doi:10.1007/s13277-015-4073-z) contains supplementary material, which is available to authorized users.…”

Section: Introductionmentioning

confidence: 99%

M2 isoform of pyruvate kinase (PKM2) is upregulated in Kazakh’s ESCC and promotes proliferation and migration of ESCC cells

et al. 2015

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The objectives of the present study are to explore role of pyruvate kinase isoenzyme type M2 (PKM2) in progression of Kazakh's esophageal squamous cell carcinoma (ESCC) in Xinjiang, China, and to clarify mechanism of PKM2 in malignant phenotype. PKM2 expression was examined using immunohistochemistry (IHC) in 101 matched pairs of ESCC and normal adjacent tissues (NATs) and using enzyme-linked immunosorbent assay (ELISA) in 35 serum samples of Kazakh's ESCC and 8 serum samples of healthy subjects. To investigate mechanism, small interfering RNA (siRNA)-PKM2 was transfected into ESCC cells. Cell migration and invasion were evaluated by wound healing and Transwell assays. Apoptosis and cell cycle were analyzed by flow cytometry (FCM). PKM2 expression was significantly higher in ESCC tissues (77.2 %, 78/101) compared with matched NAT (P = 0.003) and also higher in serum samples of Kazakh's ESCC patients (78.84 ng/mL) compared with healthy subjects (13.55 ng/mL) (P = 0.001). Patients with overexpression of PKM2 had a poor prognosis (P = 0.032). After knockdown of PKM2, cell proliferation, migration, and invasion were significantly reduced (P = 0.001), apoptosis increased (P = 0.001), and cell cycle was arrested at G1 phase. PKM2 overexpression was significantly correlated with the worse outcome of Kazakh's ESCC. Furthermore, PKM2 was involved in progression of ESCC by promoting proliferation and suppressing apoptosis, accelerating invasion, and influencing cell cycle. PKM2 could be a potential biomarker for molecular classification of ESCC.

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“…The number of detectable protein spots has increased from hundreds to thousands through advances in analytical detection of low-molecular-weight proteins [23]. In addition to gel-based techniques, mass spectrometry and highly sensitive immunodetection methods have also been successfully applied to EC proteomics [24,25] (Fig. 1).…”

Section: Introductionmentioning

confidence: 99%