Gene and miRNA expression changes in squamous cell carcinoma of larynx and hypopharynx

Nair, Jayalakshmi; Jain, Promil; Chandola, Udita; Palve, Vinayak; Vardhan, N R Harsha; Reddy, Ram Bhupal; Kekatpure, Vikram D.; Suresh, Amritha; Kuriakose, Moni Abraham; Panda, Binay

doi:10.18632/genesandcancer.69

Cited by 23 publications

(15 citation statements)

References 79 publications

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“…We previously identified a single nucleotide mutation of SCEL gene in both normal and squamous cell carcinoma of esophagus in African-Americans [52]. In our present study, SCEL is significantly under-expressed in African-American ESCC, and thus could play a role in squamous cell carcinogenesis as suggested by the down-regulation of this gene in larynx and hypopharynx [53], and in tongue squamous cell carcinoma [54]. …”

Section: Discussionsupporting

confidence: 52%

African-American esophageal squamous cell carcinoma expression profile reveals dysregulation of stress response and detox networks

Erkizan¹,

Johnson

Ghimbovschi

et al. 2017

BMC Cancer

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BackgroundEsophageal carcinoma is the third most common gastrointestinal malignancy worldwide and is largely unresponsive to therapy. African-Americans have an increased risk for esophageal squamous cell carcinoma (ESCC), the subtype that shows marked variation in geographic frequency. The molecular architecture of African-American ESCC is still poorly understood. It is unclear why African-American ESCC is more aggressive and the survival rate in these patients is worse than those of other ethnic groups.MethodsTo begin to define genetic alterations that occur in African-American ESCC we conducted microarray expression profiling in pairs of esophageal squamous cell tumors and matched control tissues.ResultsWe found significant dysregulation of genes encoding drug-metabolizing enzymes and stress response components of the NRF2- mediated oxidative damage pathway, potentially representing key genes in African-American esophageal squamous carcinogenesis. Loss of activity of drug metabolizing enzymes would confer increased sensitivity of esophageal cells to xenobiotics, such as alcohol and tobacco smoke, and may account for the high incidence and aggressiveness of ESCC in this ethnic group. To determine whether certain genes are uniquely altered in African-American ESCC we performed a meta-analysis of ESCC expression profiles in our African-American samples and those of several Asian samples. Down-regulation of TP53 pathway components represented the most common feature in ESCC of all ethnic groups. Importantly, this analysis revealed a potential distinctive molecular underpinning of African-American ESCC, that is, a widespread and prominent involvement of the NRF2 pathway.ConclusionTaken together, these findings highlight the remarkable interplay of genetic and environmental factors in the pathogenesis of African-American ESCC.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-017-3423-1) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 52%

African-American esophageal squamous cell carcinoma expression profile reveals dysregulation of stress response and detox networks

Erkizan¹,

Johnson

Ghimbovschi

et al. 2017

BMC Cancer

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“…25 miRNA-CHIP assays has indicated that many miRNAs were aberrantly expressed in CRC. 26 Several steps were involved in the biogenesis of miRNAs.…”

Section: Discussionmentioning

confidence: 99%

MiR-590-5p inhibits colorectal cancer angiogenesis and metastasis by regulating nuclear factor 90/vascular endothelial growth factor A axis

et al. 2016

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Altered expression of microRNA-590-5p (miR-590-5p) is involved in tumorigenesis, however, its role in colorectal cancer (CRC) remains to be determined. In this study, we focused on examining the effects of different expression levels of miR-590-5p in cancer cells and normal cells. Results showed that there are lower expression levels of miR-590-5p in human CRC cells and tissues than in normal control cells and tissues. Similarly, in our xenograft mouse model, knockdown of miR-590-5p promoted the progression of CRC. However, an overexpression of miR-590-5p in the mice inhibited angiogenesis, tumor growth, and lung metastasis. Nuclear factor 90 (NF90), a positive regulator of vascular endothelial growth factor (VEGF) mRNA stability and protein synthesis, was shown to be a direct target of miR-590-5p. The overexpression of NF90 restored VEGFA expression and rescued the loss of tumor angiogenesis caused by miR-590-5p. Conversely, the NF90-shRNA attenuated the increased tumor progression caused by the miR-590-5p inhibitor. Clinically, the levels of miR-590-5p were inversely correlated with those of NF90 and VEGFA in CRC tissues. Furthermore, knockdown of NF90 lead to a reduction of pri-miR-590 and an increase of mature miR-590-5p, suggesting a negative feedback loop between miR-590-5p and NF90. Collectively, these data establish miR-590-5p as an anti-onco-miR that inhibits CRC angiogenesis and metastasis through a new mechanism involving NF90/VEGFA signaling axis, highlighting the potential of miR-590-5p as a target for human CRC therapy.

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“…SCEL was enriched in stratified epithelia, where they play an important role in stress-bearing and barrier properties (8)(9)(10). Intriguingly, aberrant SCEL expression was elevated in varied malignant tumors including pancreatic cancer, colorectal cancer, and renal cancer [14][15][16] . However, it is largely unknown regarding the pathological role of SCEL in the development of GBC.…”

Section: Introductionmentioning

confidence: 99%

Role of Sciellin in gallbladder cancer proliferation and formation of neutrophil extracellular traps

et al. 2021

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Apart from primary tumor development and metastasis, cancer-associated thrombosis is the second cause of cancer death in solid tumor malignancy. However, the mechanistic insight into the development of gallbladder cancer (GBC) and cancer-associated thrombosis remains unclear. This study aimed to investigate the mechanistic role of Sciellin (SCEL) in GBC cell proliferation and the development of venous thromboembolism. The expression level of SCEL was determined by immunohistochemical staining. Roles of SCEL in gallbladder cancer cell were determined by molecular and cell biology methods. SCEL was markedly upregulated in GBC and associated with advanced TNM stages and a poor prognosis. Furthermore, SCEL interacted with EGFR and stabilized EGFR expression that activates downstream PI3K and Akt pathway, leading to cell proliferation. In addition, SCEL induces tumor cell IL-8 production that stimulates the formation of neutrophil extracellular traps (NETs), accelerating thromboembolism. In xenografts, SCEL-expressing GBCs developed larger tumors and thrombosis compared with control cells. The present results indicate that SCEL promotes GBC cell proliferation and induces NET-associated thrombosis, thus serving as a potential therapeutic target.

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Gene and miRNA expression changes in squamous cell carcinoma of larynx and hypopharynx

Cited by 23 publications

References 79 publications

African-American esophageal squamous cell carcinoma expression profile reveals dysregulation of stress response and detox networks

African-American esophageal squamous cell carcinoma expression profile reveals dysregulation of stress response and detox networks

MiR-590-5p inhibits colorectal cancer angiogenesis and metastasis by regulating nuclear factor 90/vascular endothelial growth factor A axis

Role of Sciellin in gallbladder cancer proliferation and formation of neutrophil extracellular traps

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