Knocking down Dp71 expression in A549 cells reduces its malignancy<i>in vivo</i>and<i>in vitro</i>

Tan, Sichuang; Tan, Seang‐Lin; Chen, Zhikang; Cheng, Ke; Chen, Zhicao; Wang, Wenmei; Wen, Qiaocheng; Zhang, Weilin

doi:10.3109/07357907.2015.1084002

Cited by 18 publications

(21 citation statements)

References 29 publications

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“…High DMD expression was also associated with poorer overall survival and shorter lymphocyte doubling time [17]. Other studies demonstrated that DMD Dp71 plays a central role in proliferation [6, 18], invasion and migration in vitro [18] and suppressed tumor growth in xenograft models [18]. Although the molecular mechanism underlying DMD over-expression and oncogenic activity is unknown, we suspect that it might be related to an increase expression of the Dp71 isoform.…”

Section: Discussionmentioning

confidence: 94%

Non-myogenic tumors display altered expression of dystrophin (DMD) and a high frequency of genetic alterations

et al. 2016

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DMD gene mutations have been associated with the development of Dystrophinopathies. Interestingly, it has been recently reported that DMD is involved in the development and progression of myogenic tumors, assigning DMD a tumor suppressor activity in these types of cancer. However, there are only few reports that analyze DMD in non-myogenic tumors. Our study was designed to examine DMD expression and genetic alterations in non-myogenic tumors using public repositories. We also evaluated the overall survival of patients with and without DMD mutations. We studied 59 gene expression microarrays (GEO database) and RNAseq (cBioPortal) datasets that included 9817 human samples. We found reduced DMD expression in 15/27 (56%) pairwise comparisons performed (Fold-Change (FC) ≤ 0.70; p-value range = 0.04-1.5×10−20). The analysis of RNAseq studies revealed a median frequency of DMD genetic alterations of 3.4%, higher or similar to other well-known tumor suppressor genes. In addition, we observed significant poorer overall survival for patients with DMD mutations. The analyses of paired tumor/normal tissues showed that the majority of tumor specimens had lower DMD expression compared to their normal adjacent counterpart. Interestingly, statistical significant over-expression of DMD was found in 6/27 studies (FC ≥ 1.4; p-value range = 0.03-3.4×10−15). These results support that DMD expression and genetic alterations are frequent and relevant in non-myogenic tumors. The study and validation of DMD as a new player in tumor development and as a new prognostic factor for tumor progression and survival are warranted.

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Section: Discussionmentioning

confidence: 94%

Non-myogenic tumors display altered expression of dystrophin (DMD) and a high frequency of genetic alterations

et al. 2016

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“…Cell viability was detected by Cell Counting Kit-8 (CCK-8, Beyond time, China), as previously described [ 12 ]. The assay was repeated 3 times.…”

Section: Methodsmentioning

confidence: 99%

Decreased Dp71 expression is associated with gastric adenocarcinoma prognosis

Tan

et al. 2016

Oncotarget

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For the first time, dramatically decreased Dp71 protein and mRNA was found in 34 pairs of resected primary gastric adenocarcinoma. Immunohistochemistry identified Dp71 expression suppressed in 72.2% of 104 gastric cancer patients. The decreased Dp71 expression was significantly correlated with cancer differentiation (P=0.001) and lymph vascular invasion (p=0.041). Decreased Dp71 expression was associated with a poor gastric adenocarcinoma prognosis (P=0.001). Significantly less Dp71 mRNA and protein were found in BGC823, SGC7901, AGS compared with GES-1. Via increasing lamin B1 mRNA and protein, enforced Dp71d and Dp71f expression resulted in SGC7901 proliferation inhibition. Co-IP proved interaction of Dp71 with lamin B1 in GES-1 cells. Further expression characterization showed reduced lamin B1 in gastric cancer tissue and cancer cells. Increasing lamin B1 expression results in the growth inhibition of SGC7901, which suggests that Dp71-lamin B1 protein complex plays an important role for the newly identified tumor suppressive function of Dp71.

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“…Representative images of cells migrated into the wounds were captured and the length of the scratch was recorded and calculated 48 hr later. The results show that wound closure rate = (0 hr scratch width - 48 hr scratch width/0 hr scratch width ×100 [18]. …”

Section: Methodsmentioning

confidence: 99%

“…The bottom chamber contained 700 µl medium with 20 % FBS. After 24 h, the total numbers of the Transwell assay were imaged and the number of invasive cells was evaluated by measurement of absorbance measurement at 570 nm [18]. …”

Section: Methodsmentioning

confidence: 99%

ZNF667 Serves as a Putative Oncogene in Human Hepatocellular Carcinoma

Cheng

Chen²,

Zhao

et al. 2017

Cell Physiol Biochem

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Background/Aims: Zinc finger protein 667 (ZNF667) is a member of C2H2 zinc finger protein family. For the first time, we aim to analyze the expression pattern of ZNF667 in hepatocellular carcinoma (HCC) tissues; to explore its role in HCC tumorigenesis. Methods: Immuno-histochemistry was carried out to characterize the ZNF667 expression in paraffin-embedded HCC samples. The relationship between ZNF667 expression and the clinical, pathological data of the patients were analyzed. Human normal hepatocyte cells LO2 over expressing ZNF667 (LO2-ZNF667 cells), ZNF667 depleted hepatocellular carcinoma HepG2 cells (HepG2-shZNF667 cells) were set up, their proliferation, migration and invasion abilities were analyzed. Xenograft nude mice were used to analyze the malignancy of HepG2-shZNF667 cells in vivo. Western blot was performed to analyze the expression of Bcl-2 and BAX in LO2-ZNF667 and HepG2-shZNF667 cells. Results: Increased ZNF667 was found via immuno-histochemistry in HCC. Enhanced ZNF667 expression was associated with tumor size, clinical stage and tumor differentiation. LO2-ZNF667 cells displayed increased and HepG2-shZNF667 cells decreased cell proliferation, migration and invasion. Xenograft experiments proved reduced malignancy of HepG2-shZNF667 cells in vivo. LO2-ZNF667 cells displayed increased Bcl-2 and decreased BAX protein expression. HepG2-shZNF667 cells displayed enhanced BAX and inhibited BCL-2 expression. Conclusions: ZNF667 is shown to be a new oncogene in HCC and it may serve as a new therapeutic target for HCC via enhancing BCL-2 and decreasing BAX expression.

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Knocking down Dp71 expression in A549 cells reduces its malignancyin vivoandin vitro

Cited by 18 publications

References 29 publications

Non-myogenic tumors display altered expression of dystrophin (DMD) and a high frequency of genetic alterations

Non-myogenic tumors display altered expression of dystrophin (DMD) and a high frequency of genetic alterations

Decreased Dp71 expression is associated with gastric adenocarcinoma prognosis

ZNF667 Serves as a Putative Oncogene in Human Hepatocellular Carcinoma

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