Phosphorylated AKT1 is associated with poor prognosis in esophageal squamous cell carcinoma

Zhu, Zhengfei; Yu, Weiwei; Fu, Xiaolong; Sun, Menghong; Qiao, Wei; Li, Dali; Chen, Haiquan; Xiang, Jiaqing; Li, Hecheng; Zhang, Yawei; Zhao, Wei; Zhao, Kuaile

doi:10.1186/s13046-015-0212-z

Cited by 29 publications

(34 citation statements)

References 38 publications

(34 reference statements)

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“…To further explore the mechanisms underlying miR-495-mediated inhibition of ESCC cells ability, we examined whether miR-495 targeted Akt1. Akt1 is the crucial mediator of the PI3K/Akt signaling pathway and mediates various cellular functions in a number of tumor types, including gastric cancer [18], glioma [19], lung cancer [20], and ESCC [21]. In glioma patients, overexpression of Akt protein is correlated with later glioma grade and poor prognosis [22, 23].…”

Section: Discussionmentioning

confidence: 99%

MiR-495 inhibits esophageal squamous cell carcinoma progression by targeting Akt1

et al. 2016

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MicroRNAs are involved in tumor initiation and progression by regulating oncogenes and tumor suppressor genes. Here we found that miR-495 are lower in clinical ESCC tissues than in adjacent non-tumor tissues. Moreover, the lower miR-495 expression correlated with increased lymph node metastasis (LNM), invasion and TNM stage. miR-495 overexpression predicted a favorable outcome in ESCC patients. miR-495 targeted a site in the 3′-UTR of Akt1, and miR-495 levels correlated inversely with Akt1 protein levels in ESCC tissue samples. Overexpression of miR-495 suppressed cell proliferation, blocked G1/S phase transition, and decreased migration and invasion by two ESCC cell lines in vitro and in vivo. Restoration of Akt1 protein levels in miR-495-overexpressing ESCC cells attenuated the inhibitory effects of miR-495. In addition, miR-495 suppressed cell cycle transition and the EMT signaling pathway through targeting Akt1, thereby inhibiting ESCC cell proliferation, migration, and invasion. Our results suggest that miR-495 may act as a tumor suppressor by targeting Akt1 in ESCC.

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Section: Discussionmentioning

confidence: 99%

MiR-495 inhibits esophageal squamous cell carcinoma progression by targeting Akt1

et al. 2016

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“…Also in our study, Biglycan mRNA fold expression and tissue Biglycan protein expression by IHC and western blotting in the tumour tissue were significantly higher than those in the adjacent normal tissue. Zhu et al 24 observed a twofold rise in the mRNA expression of biglycan in ESCC tissue as compared to their normal counterparts. This finding was also supported by showing a significantly higher immunostaining for Biglycan in ESCC.…”

Section: Discussionmentioning

confidence: 99%

“…22 High expression of Biglycan in malignancy has been associated with poor prognosis as observed in endometrial cancer, oesophageal cancer and gastric cancer. [23][24][25] Knockdown of Biglycan using small interfering RNA (siRNA) in HCT116 colon cancer cell line inhibited cell proliferation and produced growth arrest. 26 As it also regulates the immune system, Biglycan has been found to be associated with auto-immune diseases like systemic lupus erythematosus (SLE) where it enhances the expression of CXCL13 which is a potent B cell chemo-attractant.…”

Section: Introductionmentioning

confidence: 99%

Altered expression of small leucine-rich proteoglycans (Decorin, Biglycan and Lumican): Plausible diagnostic marker in urothelial carcinoma of bladder

et al. 2017

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Small leucine-rich proteoglycans are components of extracellular matrix that regulates neoplastic transformation. Among small leucine rich proteoglycans, Decorin, Biglycan and Lumican are most commonly implicated markers, and their expression is well studied in various malignancies. In this novel study, we have collectively evaluated expression of these three molecules in urothelial carcinoma of bladder. Thirty patients of confirmed untreated bladder cancer, 30 healthy controls for blood and 30 controls for adjacent non-tumour tissue were enrolled. Blood was collected from all subjects and tumour/adjacent normal tissue was obtained from the patients. Circulatory levels were estimated by enzyme-linked immunosorbent assay, relative messenger RNA expression by quantitative polymerase chain reaction and protein expression by immunohistochemistry and western-blotting. Circulatory levels of Biglycan (p = 0.0038) and Lumican (p < 0.0001) were significantly elevated, and that of Decorin (p < 0.0001) was significantly reduced in patients as compared with controls. Protein expression by immunohistochemistry and western-blotting showed elevated expression of Lumican and Biglycan and lower expression of Decorin in urothelial carcinoma of bladder. Quantitative polymerase chain reaction for messenger RNA expression from tissue specimens revealed significantly higher expression of Biglycan (p = 0.0008) and Lumican (p = 0.01) and lower expression of Decorin (p < 0.0001) in urothelial carcinoma of bladder. Out of all molecules receiver operating characteristic curve showed that the 0.207 ng/ml cut-off of serum Lumican provided optimum sensitivity (90.0%) and specificity (90.0%). Significant alteration of matrix small leucine-rich proteoglycans in urothelial carcinoma of bladder was observed. Higher expression of Lumican in Bladder cancer patients with the cut-off value of highest optimum sensitivity and specificity shows its importance as a potential non-invasive marker for early detection of UBC following further validation in large patient cohort.

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“…However, biglycan expression and serological levels of its processed byproducts correlate with the extent of liver fibrosis in murine models (108,204). Biglycan is also involved with progression and poor prognosis in a variety of malignancies such as gastrointestinal and endometrial cancers (7,122,221,377,415). In contrast, biglycan expression correlates with a favorable prognosis in bladder cancer where it seems to have an inhibitory effect on tumor cell proliferation (266).…”

Section: Proteoglycansmentioning

confidence: 99%

The wound healing, chronic fibrosis, and cancer progression triad

Rybinski

Franco‐Barraza

Cukierman

2014

Physiological Genomics

208

175

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For decades tumors have been recognized as “wounds that do not heal.” Besides the commonalities that tumors and wounded tissues share, the process of wound healing also portrays similar characteristics with chronic fibrosis. In this review, we suggest a tight interrelationship, which is governed as a concurrence of cellular and microenvironmental reactivity among wound healing, chronic fibrosis, and cancer development/progression (i.e., the WHFC triad). It is clear that the same cell types, as well as soluble and matrix elements that drive wound healing (including regeneration) via distinct signaling pathways, also fuel chronic fibrosis and tumor progression. Hence, here we review the relationship between fibrosis and cancer through the lens of wound healing.

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Phosphorylated AKT1 is associated with poor prognosis in esophageal squamous cell carcinoma

Cited by 29 publications

References 38 publications

MiR-495 inhibits esophageal squamous cell carcinoma progression by targeting Akt1

MiR-495 inhibits esophageal squamous cell carcinoma progression by targeting Akt1

Altered expression of small leucine-rich proteoglycans (Decorin, Biglycan and Lumican): Plausible diagnostic marker in urothelial carcinoma of bladder

The wound healing, chronic fibrosis, and cancer progression triad

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