Derlin-1 is overexpressed in human colon cancer and promotes cancer cell proliferation

Tan, Xueming; He, Xiaolu; Jiang, Zhonghua; Wang, Xiaohong; Ma, Limei; Liu, Li; Wang, Xiang; Fan, Zhining; Su, Dongming

doi:10.1007/s11010-015-2496-x

Cited by 35 publications

(37 citation statements)

References 24 publications

(46 reference statements)

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“…These data demonstrate that the levels of Derlin-1 protein expression were elevated in the majority of BC tissues compared with normal bladder tissues. Our results are consistent with those of previous studies showing that Derlin-1 is overexpressed in various types of human cancers [13–15, 27]. …”

Section: Discussionsupporting

confidence: 94%

“…Almost all solid tumors growth depends on an intact unfolded protein response and tolerance of ER stress, such as hypoxia [24–26]. In human breast, lung, and colon cancer, several lines of direct evidence demonstrated a significant association between Derlin-1 up-regulation and tumor grade, as well as between Derlin-1 up-regulation and lymph node metastasis [14, 15, 27]. …”

Section: Discussionmentioning

confidence: 99%

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High Expression of Derlin-1 Is Associated with the Malignancy of Bladder Cancer in a Chinese Han Population

Wang

Zhang

et al. 2016

PLoS ONE

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Derlin-1 is overexpressed in various types of solid tumors and has an important function in cancer progression. However, its expression pattern in and association with the clinicopathological characteristics of human bladder cancer remain unclear. In the present study, 3 pairs of fresh samples of bladder cancer tissue and paracancerous tissue were first detected by liquid chromatography tandem mass spectrometry (UPLC-MS/MS) to screen for differentially expressed proteins. Following bioinformatics analysis and assessments by qRT-PCR and western blotting, Derlin-1 was selected as a candidate protein and was then validated in samples from patients with bladder cancer by immunohistochemistry and western blotting. The results showed that the bladder cancer tissues exhibited higher levels of Derlin-1 expression than the paracancerous tissues (P < 0.05). Positive expression of Derlin-1 was significantly correlated with tumor stage, histological grade, and lymph node metastasis (P < 0.001) but was not correlated with other clinicopathological parameters including patient age (P = 0.758) and gender (P = 0.831). Besides, Derlin-1 was highly expressed in BC cell lines (um-uc-3 and T24), and the interference of Derlin-1 could reverse EMT progression, inhibit the tumor migration and invasion in T24 cells. Further, patients with positive Derlin-1 expression had shorter overall survival than those with negative expression (P < 0.001). Taken together, our results demonstrated that Derlin-1 was overexpressed in bladder cancer and was associated with the malignancy of bladder cancer.

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Section: Discussionsupporting

confidence: 94%

Section: Discussionmentioning

confidence: 99%

High Expression of Derlin-1 Is Associated with the Malignancy of Bladder Cancer in a Chinese Han Population

Wang

Zhang

et al. 2016

PLoS ONE

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“…Moreover, experiments of double-transfection by upregulating DERL1 in miR-181d-overexpressed ESCC cells revealed that DERL1 reversed the tumor suppression of miR-181d overexpression on ESCC proliferation, migration and cell cycle transition. DERL1 was often found to be overexpressed in human cancers, including colon (15), lung (17) or pancreatic cancer (16). Thus, our data are in line with previous studies, showing that DERL1 could be an active oncogenic gene in various types of human cancers, including ESCC.…”

Section: Discussionsupporting

confidence: 92%

“…In human cancers, DERL1 has been mostly reported to be an oncogene of regulating carcinoma progression. In colon cancer, DERL1 was upregulated in carcinoma tissues and promoted cancer proliferation (15).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-181d is a tumor suppressor in human esophageal squamous cell carcinoma inversely regulating Derlin-1

Shi

et al. 2016

Oncology Reports

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Esophageal squamous cell carcinoma (ESCC) is the predominant subtype of human esophageal cancer in East Asia. In the present study, we explored the tumor suppressive function of microRNA-181d (miR-181d) in ESCC. Quantitative RT-PCR was used to assess gene levels of miR‑181d in both ESCC cell lines and clinical samples. Lentiviral transduction was used to overexpress miR-181d in ECA109 and Kyse30 cells. The possible tumor suppressive effects of miR-181d overexpression on ESCC proliferation, migration and cell cycle transition in vitro, and tumorigenicity in vivo were examined. Downstream target gene of miR‑181d in ESCC, Derlin-1 (DERL1) was assessed by luciferase assay and qRT-PCR. DERL1 was also force expressed in miR‑181d-overexperssed ECA109 and Kyse30 cells to evaluate its reverse effect on miR-181d mediated tumor suppression in ESCC. miR-181d was aberrantly downregulated in both ESCC cell lines and human tumors. Lentivirus-mediated miR-181d overexpression had significant tumor suppressing functions by inhibiting cancer proliferation, migration and arresting cell cycle transition in vitro, as well as inhibiting tumorigenicity in vivo. DERL1 was identified as downstream target gene of miR-181d in ESCC cells. Forced overexpression of DERL1 in ESCC cells was shown to greatly reverse the tumor suppressive effects of miR-181d upregulation on ESCC in vitro proliferation, migration and cell cycle arrest. Out data suggest that miR-181d is a tumor suppressor in ESCC inversely regulating its downstream target gene of DERL1.

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“…We identified DERL1 as a direct downstream target gene of miR-598 using bioinformatics method that was further confirmed by the luciferase reporter assay. DERL1 is overexpressed in NSCLC; it also promotes cancer cell invasion via EGFR-ERK-mediated upregulation of MMP-2 and MMP-9 [16, 19, 21]. However, the correlation between DERL1 and miR-598 remains unclear.…”

Section: Discussionmentioning

confidence: 99%

MiR-598 Suppresses Invasion and Migration by Negative Regulation of Derlin-1 and Epithelial-Mesenchymal Transition in Non-Small Cell Lung Cancer

Yang

Wei

Qin

et al. 2018

Cell Physiol Biochem

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Background/Aims: MicroRNAs regulate a wide range of biological processes of non-small cell lung cancer (NSCLC). Although miR-598 has been reported to act as a suppressor in osteosarcoma and colorectal cancer, the physiological function of miR-598 in NSCLC remains unknown. In this study, the role of miR-598 in NSCLC was investigated. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to estimate the expression of miR-598 and Derlin-1 (DERL1) in both NSCLC tissues and cell lines. Immunohistochemistry (IHC) analyzed the association between the miR-598 expression and epithelial-mesenchymal transition (EMT) hallmark genes (E-cadherin, Vimentin) by staining the tumors representative of the high- and low-expression groups. The effect of miR-598 and DERL1 on invasion and migration was determined in vitro using transwell and wound-healing assays. The molecular mechanism underlying the relevance between miR-598 and DERL1 was elucidated by luciferase assay and Western blot. Western blot assessed the expression levels of EMT hallmark genes in cell lines. Xenograft tumor formation assay was conducted as an in vivo experiment. Results: In this study, a relatively low level of miR-598 and high DERL1 expressions were found in NSCLC specimens and cell lines. IHC results established a positive correlation between the miR-598 expression and E-cadherin and a negative with Vimentin. DERL1 was verified as a direct target of miR-598 by luciferase assay. In vitro, the over-expression of miR-598 negatively regulated DERL1 and EMT for the suppression of invasion and migration. In vivo, the over-expression of miR-598 could inhibit tumor cell metastasis in NSCLC. Conclusions: These findings for the first time revealed that miR-598, as a tumor suppressor, negatively regulate DERL1 and EMT to suppress the invasion and migration in NSCLC, thereby putatively serving as a novel therapeutic target for NSCLC clinical treatment.

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Derlin-1 is overexpressed in human colon cancer and promotes cancer cell proliferation

Cited by 35 publications

References 24 publications

High Expression of Derlin-1 Is Associated with the Malignancy of Bladder Cancer in a Chinese Han Population

High Expression of Derlin-1 Is Associated with the Malignancy of Bladder Cancer in a Chinese Han Population

MicroRNA-181d is a tumor suppressor in human esophageal squamous cell carcinoma inversely regulating Derlin-1

MiR-598 Suppresses Invasion and Migration by Negative Regulation of Derlin-1 and Epithelial-Mesenchymal Transition in Non-Small Cell Lung Cancer

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