Overexpression of malignant brain tumor domain containing protein 1 predicts a poor prognosis of prostate cancer

Wu, Wanhua; Bai, Shoumei; Zhu, Dingjun; Li, Kaiwen; Dong, Wen; Wang, He; Peng, Shengmeng; Lai, Yue‐Yun; Wang, Qiong; Guo, Zhanfang; Liu, Leyuan; Huang, Hai

doi:10.3892/ol.2019.10109

Cited by 7 publications

(4 citation statements)

References 27 publications

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“…For example, Luo et al (2013) showed that depletion of MBTD1 in oocytes activated the cell cycle checkpoint protein Chk1 and led to cell cycle arrest. Further, regulation of HESC proliferation by MBTD1 is in line with published work that indicated that MBTD1 controls growth of multiple cancer cells (de Rooij et al, 2016;Hoang et al, 2018;Yamamoto et al, 2018;Fu et al, 2019;Plesa and Sujobert, 2019;Wu et al, 2019). Thus, based on our findings and published work, we posit that MBTD1 functions in HESC decidualization through multiple cellular mechanisms.…”

Section: Discussionsupporting

confidence: 90%

A Role for Malignant Brain Tumor Domain-Containing Protein 1 in Human Endometrial Stromal Cell Decidualization

Chadchan

Maurya

Krekeler

et al. 2020

Front. Cell Dev. Biol.

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Up to 30% of women experience early miscarriage due to impaired decidualization. For implantation to occur, the uterine endometrial stromal fibroblast-like cells must differentiate into decidual cells, but the genes required for decidualization have not been fully defined. Here, we show that Malignant Brain Tumor Domain-containing Protein 1 (MBTD1), a member of the polycomb group protein family, is critical for human endometrial stromal cell (HESC) decidualization. MBTD1 predominantly localized to HESCs during the secretory phase and the levels were significantly elevated during in vitro decidualization of both immortalized and primary HESCs. Importantly, siRNA-mediated MBTD1 knockdown significantly impaired in vitro decidualization of both immortalized and primary HESCs, as evidenced by reduced expression of the decidualization markers PRL and IGFBP1. Further, knockdown of MBTD1 reduced cell proliferation and resulted in G2/M cell cycle arrest in decidualizing HESCs. Although progesterone signaling is required for decidualization, MBTD1 expression was not affected by progesterone signaling; however, MBTD1 knockdown significantly reduced expression of the progesterone target genes WNT4, FOXOA1, and GREB1. Collectively, our data suggest that MBTD1 contributes to in vitro decidualization of HESCs by sustaining progesterone signaling. This work could have implications for designing diagnostic and therapeutic tools for recurrent pregnancy loss.

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Section: Discussionsupporting

confidence: 90%

A Role for Malignant Brain Tumor Domain-Containing Protein 1 in Human Endometrial Stromal Cell Decidualization

Chadchan

Maurya

Krekeler

et al. 2020

Front. Cell Dev. Biol.

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“…Furthermore, we found that circZNF236 was able to absorb miR-145-5p to increase the expression of MBTD1. In line with this observation, MBTD1 expression has been shown to be enhanced in prostate cancer tissues and is associated with aggressive clinicopathological characteristics [27] . Indeed, we found that increased expression of MBTD1 could rescue the inhibitory effects of circZNF236 silencing on malignant properties of OSCC cells.…”

Section: Discussionmentioning

confidence: 73%

CircZNF236 facilitates malignant progression in oral squamous cell carcinoma by sequestering miR-145-5p

Lü

Che

et al. 2023

Clin Transl Oncol

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BackgroundA number of non-coding circular RNAs (circRNAs) have recently been implicated in the modulation of gene expression in cancer models. We therefore sought to explore if circZNF236 has a role in oral squamous cell carcinoma (OSCC). MethodsWe rst examined circZNF236 expression in 32 pairs of OSCC and noncancerous tissues. We then investigated a functional role for circZNF236 using knockdown and overexpression approaches in OSCC cancer cell lines. Cell counting kit-8, wound healing, Transwell, and ow cytometry were employed to assess circZNF236 function in vitro. The association between circZNF236 and miR-145-5p, or that between miR-145-5p and malignant brain tumour domain containing 1 (MBTD1) was predicted by bioinformatics and demonstrated by dual-luciferase reporter assays, RNA pull-down assays as well as RNA immunoprecipitation (RIP) assays. A mouse OSCC xenograft model was employed to demonstrate the impacts of circZNF236 inhibition on tumor development in vivo. ResultsOSCC tissues and cells had higher levels of circZNF236 expression compared with normal controls. Furthermore, high circZNF2361 levels in patients with OSCC correlated with a poor prognosis.CircZNF236 silencing decreased the malignant properties of OSCC cells and suppressed OSCC tumor formation in the mouse model. We then noticed that miR-145-5p can be regulated by circZNF236, and that circZNF2361 promoted OSCC development by absorbing miR-145-5p and consequently upregulating MBTD1 expression. ConclusionCircZNF236 modulates OSCC via an miR-145-5p/MBTD1 axis. These results support the potential of circZNF236 as a treatment target for OSCC.

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“…The percentage of positive cells was scored as follows: <5% (score: 0), 6-25% (score:1), 26-50% (score: 2), 51-75% (score: 3) and >75% (score: 4). The immunoreactivity scores (IRS) were calculated by adding the immunostaining percentages and immunostaining intensity scores together [28].…”

Section: Evaluation Of Immunostaining Resultsmentioning

confidence: 99%

Noxa and Puma genes regulated by hTERT promoter can mitigate growth and induce apoptosis in hepatocellular carcinoma mouse model

Zhao

et al. 2022

J. Cancer

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With significant high incidence and death rates, liver cancer has become one of the most common cancers all over the world. Hence, novel strategies are needed for the management of this malignancy. Apoptotic related proteins Noxa and Puma are the members of BH3-only family. In this study, human Noxa or Puma coding sequences have been inserted into plasmid pcDNA 3.1 regulated by human TERT promoter. The transfection of HepG2 cells with pcTERT-Noxa or pcTET-Puma resulted in the significant suppression of cell proliferation as well as finally led to apoptosis via mitochondrial and death receptor pathways, and also exhibited significantly reduced the ability of invasion and metastasis. Moreover, an in vivo study revealed that intratumoral injections of pcTERT-Noxa or pcTERT-Puma plasmids effectively suppressed the tumor growth and can exhibit anti-neoplastic effects by recruiting CD3, CD8, CD45 positive T lymphocytes in the tumor tissues. Overall, our findings illustrated that pcTERT-Noxa and pcTERT-Puma may exhibit significant anti-tumor effects both in vivo and in vivo.

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Overexpression of malignant brain tumor domain containing protein 1 predicts a poor prognosis of prostate cancer

Cited by 7 publications

References 27 publications

A Role for Malignant Brain Tumor Domain-Containing Protein 1 in Human Endometrial Stromal Cell Decidualization

A Role for Malignant Brain Tumor Domain-Containing Protein 1 in Human Endometrial Stromal Cell Decidualization

CircZNF236 facilitates malignant progression in oral squamous cell carcinoma by sequestering miR-145-5p

Noxa and Puma genes regulated by hTERT promoter can mitigate growth and induce apoptosis in hepatocellular carcinoma mouse model

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