Comparative proteomic analysis of oral squamous cell carcinoma and adjacent non-tumour tissue from Thailand

Chanthammachat, Pitak; Promwikorn, Waraporn; Pruegsanusak, Kowit; Roytrakul, Sittiruk; Srisomsap, Chantragan; Chokchaichamnankit, Daranee; Svasti, Jisnuson; Boonyaphiphat, Pleumjit; Singkhamanan, Kamonnut; Thongsuksai, Paramee

doi:10.1016/j.archoralbio.2013.08.002

Cited by 28 publications

(31 citation statements)

References 32 publications

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“…HSPA8, also known as heat shock cognate 71 kDa protein or HSC71, is a constitutively expressed protein encoded by the HSPA8 gene on chromosome 11 in humans . However, overexpression of HSPA8 has been observed in various cancers like colorectal cancer and oral squamous cell carcinoma . In fact, it has been identified as a candidate biomarker for endometrial carcinoma .…”

Section: Discussioncontrasting

confidence: 41%

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miR‐26b‐5p helps in EpCAM+cancer stem cells maintenance via HSC71/HSPA8 and augments malignant features in HCC

Khosla

Hemati

Rastogi

et al. 2019

Liver International

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Background Targeting cancer stem cells (CSCs) in hepatocellular carcinoma (HCC) is difficult because of their similarities with normal stem cells (NSCs). EpCAM can identify CSCs from EpCAM+AFP+HCC cases, but is also expressed on NSCs. We aimed to distinguish the two using integrated protein, mRNA and miRNA profiling. Methods iTRAQ based protein profiling and Next Generation Sequencing (NGS) was performed on EpCAM+/EpCAM− cells isolated from HCC (Ep+CSC, Ep−HCC) and EpCAM+ cells from non‐cancerous/non‐cirrhotic control liver tissues (Ep+NSC). Validations were done using qRT‐PCR, flowcytometry and western blotting followed by in vitro and in vivo functional studies. Results 11 proteins were overexpressed (>3 fold) in Ep+CSCs compared to Ep−HCC and Ep+NSC cells. However, RNA‐sequencing confirmed the Ep+CSC specific up‐regulation of only HSPA8, HNRNPC, MPST and GAPDH mRNAs among these. Database search combined with miRNA profiling revealed Ep+CSC specific down‐regulation of 29 miRNAs targeting these four genes. Of these, only miR‐26b‐5p was found to target both HSPA8 and EpCAM. Validation of HSPA8 overexpression and miR‐26b‐5p down‐regulation followed by linear regression analysis established a negative correlation between the two. Functional studies demonstrated that reduced miR‐26b‐5p expression increased the spheroid formation, migration, invasion and tumourigenicity of Ep+CSCs. Furthermore, anti‐miR‐26b‐5p increased the number of Ep+CSCs with a concomitant overexpression of stemness genes and reduction of proapoptotic protein BBC3, which is a known substrate of HSPA8. Conclusion miR‐26b‐5p imparts metastatic properties and helps in maintenance of Ep+CSCs via HSPA8. Thus, miR‐26b‐5p and HSPA8 could serve as molecular targets for selectively eliminating the Ep+CSC population in human HCCs.

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Section: Discussioncontrasting

confidence: 41%

“…37 However, overexpression of HSPA8 has been observed in various cancers like colorectal cancer and oral squamous cell carcinoma. 38,39 In fact, it has been identified as a candidate biomarker for endometrial carcinoma. 40 Additionally, HSPA8 was shown to be up-regulated in HBV-related HCC cases.…”

Section: Discussionmentioning

confidence: 99%

miR‐26b‐5p helps in EpCAM+cancer stem cells maintenance via HSC71/HSPA8 and augments malignant features in HCC

Khosla

Hemati

Rastogi

et al. 2019

Liver International

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“…KIAA1199 had been identified not only to be associated with clinicopathological parameters and 5 year-overall survival rate in colon cancer but also as an essential inducer for cell proliferation, migration and invasion by complex signaling pathways[9–11]. Proteomics analysis by two-dimensional gel electrophoresis and mass spectrometry assay revealed KIAA1199 was one novel protein that expressed abnormally in oral cancer, which was then demonstrated by Realtime-PCR assay [6]. Furthermore, the latest report also indicated KIAA1199 as a newly identified protein which probably played significant role in pancreatic ductal adenocarcinoma [7].…”

Section: Introductionmentioning

confidence: 99%

KIAA1199 promotes migration and invasion by Wnt/β-catenin pathway and MMPs mediated EMT progression and serves as a poor prognosis marker in gastric cancer

Jia

Wang

et al. 2017

PLoS ONE

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BackgroundKIAA1199 was upregulated in diverse cancers, but the association of KIAA1199 with gastric cancer (GC), the biological role of KIAA1199 in GC cells and the related molecular mechanisms remain to be elucidated.MethodsKIAA1199 expression was analysed by reverse transcription-polymerase chain reaction assay (RT-PCR) and immunohistochemistry (IHC) in GC patient tissue. The small hairpin RNA (shRNA) was applied for the knockdown of endogenous KIAA1199 in NCI-N87 and AGS cells. MTT, colony formation, scratch wounding migration, transwell chamber migration and invasion assays were employed respectively to investigate the role of KIAA1199 in GC cells. The potential signaling pathway of KIAA1199 induced migration and invasion was detected.ResultsKIAA1199 was upregulated in GC tissue and was an essential independent marker for poor prognosis. Knockdown KIAA1199 suppressed the proliferation, migration and invasion in GC cells. KIAA1199 stimulated the Wnt/β-catenin signaling pathway and the enzymatic activity of matrix metalloproteinase (MMP) family members and thus accelerated the epithelial-to-mesenchymal transition (EMT) progression in GC cells.ConclusionThese findings demonstrated that KIAA1199 was upregulated in GC tissue and associated with worse clinical outcomes in GC, and KIAA1199 acted as an oncogene by promoting migration and invasion through the enhancement of Wnt/β-catenin signaling pathway and MMPs mediated EMT progression in GC cells.

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“…nUPLC-UDMS E discovery-driven analysis offers a unique avenue to discover proteins and pathways that are previously not known to be altered in OSCC. Previously, studies using non-pooled paired healthy and OSCC tissue samples for direct comparison with MS have used a gel-based matrix to register the differences between the cases and controls after which protein spots are identified using MS [12][13][14]. However, shotgun proteomics, as done here, and the electrophoresis approaches have different scopes and limitations.…”

Section: Introductionmentioning

confidence: 99%

Label-free tissue proteomics can classify oral squamous cell carcinoma from healthy tissue in a stage-specific manner

et al. 2018

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No prognostic or predictive biomarkers for oral squamous cell carcinoma (OSCC) exist. We aimed to discover novel proteins, altered in OSCC, to be further investigated as potential biomarkers, and to improve understanding about pathways involved in OSCC. Materials and Methods: Proteomic signatures of seven paired healthy and OSCC tissue samples were identified using ultra-definition quantitative mass spectrometry, then analysed and compared using Anova, principal component analysis, hierarchical clustering and OPLS-DA modelling. A selection of significant proteins that were also altered in the serum from a previous study (PMID: 28632724) were validated immunohistochemically on an independent cohort (n = 66) to confirm immunopositivity and location within tumour tissue. Ingenuity Pathways Analysis was employed to identify altered pathways. Results: Of 829 proteins quantified, 257 were significant and 72 were able to classify healthy vs OSCC using OPLS-DA modelling. We identified 19 proteins not previously known to be upregulated in OSCC, including prosaposin and alpha-taxilin. KIAA1217 and NDRG1 were upregulated in stage IVa compared with stage I tumours. Altered pathways included calcium signalling, cellular movement, haematological system development and function, and immune cell trafficking, and involved NF-kB and MAPK networks. Conclusions: We found a set of proteins reliably separating OSCC tumour from healthy tissue, and multiple proteins differing between stage I and stage IVa OSCC. These potential biomarkers can be studied and validated in larger cohorts.

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Comparative proteomic analysis of oral squamous cell carcinoma and adjacent non-tumour tissue from Thailand

Cited by 28 publications

References 32 publications

miR‐26b‐5p helps in EpCAM+cancer stem cells maintenance via HSC71/HSPA8 and augments malignant features in HCC

miR‐26b‐5p helps in EpCAM+cancer stem cells maintenance via HSC71/HSPA8 and augments malignant features in HCC

KIAA1199 promotes migration and invasion by Wnt/β-catenin pathway and MMPs mediated EMT progression and serves as a poor prognosis marker in gastric cancer

Label-free tissue proteomics can classify oral squamous cell carcinoma from healthy tissue in a stage-specific manner

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