Gene Expression Profile of Stromal Factors in Cancer-Associated Fibroblasts from Prostate Cancer

Eiró, Noemí; Fernandez-Gomez, Jesus; León, C. González-Ruiz de; Fraile, María; Gonzalez-Suarez, Jorge; Lobo-Rodríguez, Beatriz; J, García Rodríguez; Escaf, Safwan; Vizoso, F

doi:10.3390/diagnostics12071605

Cited by 9 publications

(4 citation statements)

References 36 publications

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“…Cellular matrix metalloproteins are key factors in cancer cell metastasis and drug resistance. In prostate cancer studies, MMP2 and MMP9 were found to be involved in prostate cancer invasion [ 14 ], and both were involved in the development of drug resistance in prostate cancer [ 15 ]. In liver cancer studies, the upregulation of MMP2 and MMP9 expression enhanced the migration and proliferation ability of liver cancer cells [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

ADAR1 affects gastric cancer cell metastasis and reverses cisplatin resistance through AZIN1

Wang

et al. 2023

Anti-Cancer Drugs

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Adenosine deaminases acting on RNA1 (ADAR1) are involved in the occurrence and development of cancers. Although the role of ADAR1 in gastric cancer metastasis has been reported, the role of ADAR1 in the mechanism of cisplatin resistance in gastric cancer is not clear. In this study, human gastric cancer tissue specimens were used to construct cisplatin-resistant gastric cancer cells; the results indicated that the mechanism underlying the inhibition of gastric cancer metastasis and reversal of cisplatin-resistant gastric cancer by ADAR1 inhibits gastric cancer occurs through the antizyme inhibitor 1 (AZIN1) pathway. We assessed ADAR1 and AZIN1 expression in the tissues of patients with low to moderately differentiated gastric cancer. Gastric cancer cells (human gastric adenocarcinoma cell line [AGS] and HGC-27 cells) and gastric cancer cisplatin-resistant cells (AGSCDDP and HGC-27CDDP) were selected, and the protein expression of ADAR1 and AZIN1 was detected using immunocytochemistry and immunocytofluorescence. The effects of ADAR1 small interfering RNA (siRNA) on the invasion, migration and proliferation of cisplatin-resistant gastric cancer cells were investigated. Western blot assays were used to assess the protein expression levels of ADAR1, AZIN1 and epithelial–mesenchymal transition (EMT)-related markers. In-vivo experiments, a subcutaneous tumor formation model of nude mice was established, and the effects of ADAR1 on tumor growth and AZIN1 expression level were detected by hematoxylin and eosin, immunohistochemistry and western blot. The expression of ADAR1 and AZIN1 in human gastric cancer tissue was significantly higher than that in paracancerous tissues. The colocalization of ADAR1, AZIN1 and E-cadherin expression in immunofluorescence assays indicated a significant correlation between the three. In in-vitro experiments, ADAR1 knockout not only reduced the invasion and migration ability of AGS and HGC-27 cells but also reduced that of cisplatin-resistant gastric cancer cells. ADAR1 siRNA inhibited the proliferation and decreased the colony number of cisplatin-resistant gastric cancer cells. ADAR1 siRNA decreased the expression of AZIN1 and EMT-related marker proteins (vimentin, N-cadherin, β-catenin, MMP9, MMP2 and TWIST). The effect of ADAR1 siRNA combined with AZIN1 siRNA was more significant. In-vivo, the knockdown of ADAR1 significantly inhibited tumor growth and AZIN1 expression. ADAR1 and AZIN1 are antimetastatic targets of gastric cancer, and AZIN1 is a downstream regulatory target of ADAR1. ADAR1 knockout can inhibit the metastasis of gastric cancer cells and reverse the cisplatin resistance of gastric cancer cells by downregulating the expression of AZIN1, potentially resulting in increased treatment efficacy.

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Section: Discussionmentioning

confidence: 99%

ADAR1 affects gastric cancer cell metastasis and reverses cisplatin resistance through AZIN1

Wang

et al. 2023

Anti-Cancer Drugs

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“…Another study showed that HEYL expression correlated with the stromal transformation of the TME [52]. Upon its overexpression, transcriptional activation of cadherin 11 (CDH11) was observed [52], which was linked with stroma-epithelium interaction [53]. Another gene in the SU-SD signature ACTA2 (alpha)-SMA is a specific marker for myofibroblasts and is a hallmark of myofibroblast differentiation [54,55].…”

Section: Discussionmentioning

confidence: 99%

A Novel Gene List Identifies Tumors with a Stromal-Mesenchymal Phenotype and Worse Prognosis in Gastric Cancer

Canli

Uner

Kucukkaraduman

et al. 2023

Cancers

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Background: Molecular biomarkers that predict disease progression can help identify tumor subtypes and shape treatment plans. In this study, we aimed to identify robust biomarkers of prognosis in gastric cancer based on transcriptomic data obtained from primary gastric tumors. Methods: Microarray, RNA sequencing, and single-cell RNA sequencing-based gene expression data from gastric tumors were obtained from public databases. Freshly frozen gastric tumors (n = 42) and matched FFPE (formalin-fixed, paraffin-embedded) (n = 40) tissues from a Turkish gastric cancer cohort were used for quantitative real-time PCR and immunohistochemistry-based assessments of gene expression, respectively. Results: A novel list of 20 prognostic genes was identified and used for the classification of gastric tumors into two major tumor subgroups with differential stromal gene expression (“Stromal-UP” (SU) and “Stromal-DOWN” (SD)). The SU group had a more mesenchymal profile with an enrichment of extracellular matrix-related gene sets and a poor prognosis compared to the SD group. Expression of the genes within the signature correlated with the expression of mesenchymal markers ex vivo. A higher stromal content in FFPE tissues was associated with shorter overall survival. Conclusions: A stroma-rich, mesenchymal subgroup among gastric tumors identifies an unfavorable clinical outcome in all cohorts tested.

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“…[30,31] Besides, CDH11 has been implicated in breast, prostate, colorectal cancer metastases. [32][33][34] However, based on recent studies, CDH11 functions as a gene that suppresses tumors, upon CDH11 inactivation, which is linked to the malignant characteristics of different human tumors. [35,36] However, the association of CDH11 with BC is yet to be fully elucidated.…”

Section: Discussionmentioning

confidence: 99%

Identifying stage-associated hub genes in bladder cancer via weighted gene co-expression network and robust rank aggregation analyses

Feng

Zhong²,

Jian-hua³

et al. 2022

Medicine

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Background: Bladder cancer (BC) is among the most frequent cancers globally. Although substantial efforts have been put to understand its pathogenesis, its underlying molecular mechanisms have not been fully elucidated. Methods: The robust rank aggregation approach was adopted to integrate 4 eligible bladder urothelial carcinoma microarray datasets from the Gene Expression Omnibus. Differentially expressed gene sets were identified between tumor samples and equivalent healthy samples. We constructed gene co-expression networks using weighted gene co-expression network to explore the alleged relationship between BC clinical characteristics and gene sets, as well as to identify hub genes. We also incorporated the weighted gene co-expression network and robust rank aggregation to screen differentially expressed genes. Results: CDH11, COL6A3, EDNRA, and SERPINF1 were selected from the key module and validated. Based on the results, significant downregulation of the hub genes occurred during the early stages of BC. Moreover, receiver operating characteristics curves and Kaplan–Meier plots showed that the genes exhibited favorable diagnostic and prognostic value for BC. Based on gene set enrichment analysis for single hub gene, all the genes were closely linked to BC cell proliferation. Conclusions: These results offer unique insight into the pathogenesis of BC and recognize CDH11, COL6A3, EDNRA, and SERPINF1 as potential biomarkers with diagnostic and prognostic roles in BC.

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Gene Expression Profile of Stromal Factors in Cancer-Associated Fibroblasts from Prostate Cancer

Cited by 9 publications

References 36 publications

ADAR1 affects gastric cancer cell metastasis and reverses cisplatin resistance through AZIN1

ADAR1 affects gastric cancer cell metastasis and reverses cisplatin resistance through AZIN1

A Novel Gene List Identifies Tumors with a Stromal-Mesenchymal Phenotype and Worse Prognosis in Gastric Cancer

Identifying stage-associated hub genes in bladder cancer via weighted gene co-expression network and robust rank aggregation analyses

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