Disruption of oncogenic liver-intestine cadherin (CDH17) drives apoptotic pancreatic cancer death

Liu, Xinjian; Huang, Yue; Hao, Yuan; Qi, Xiaoqiang; Manjunath, Yariswamy; Avella, Diego M.; Kaifi, Jussuf T.; Miao, Yi; Li, Min; Jiang, Kuirong; Li, Guangfu

doi:10.1016/j.canlet.2019.04.022

Cited by 24 publications

(28 citation statements)

References 31 publications

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“…Tumor tissue sections were harvested and treated as previously described 31 . Primary antibodies for anti-human ASF1B (1:100), anti-mouse ASF1B, Ki67, and CD31 (1:100) were purchased from Cell Signaling Technologies.…”

Section: Immunohistochemistrymentioning

confidence: 99%

ASF1B promotes cervical cancer progression through stabilization of CDK9

et al. 2020

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Cervical cancer (CC) is one of the most deadly cancers in women, its current treatments still result in poor outcomes and developing the novel targets and therapeutic strategies are urgently needed. Recent studies have shown that anti-silencing function 1B (ASF1B) might be used as a new proliferation marker for cancer diagnosis and prognosis. However, the expression and function of ASF1B in cervical cancer remain unclear. Here, we induced ASF1B knockdown and overexpression in cervical cancer cell lines and detected the biological behavior changes in vitro. Furthermore, we established two murine models using stable ASF1B-shRNA HeLa cells or normal HeLa cells following AAV-shRNA-ASF1B administration to evaluate how suppression of ASF1B affects tumor growth. We showed that ASF1B functions as an oncogene in cervical cancer cells. Silence of ASF1B suppressed cervical cancer cell growth in vitro and in vivo, while, ASF1B overexpression accelerated cancer cell proliferation. Furthermore, ASF1B deficiency induced cell cycle arrest and apoptosis. Mechanistically, we found that ASF1B formed stable complexes with cyclin-dependent kinase 9 (CDK9), and positively regulated CDK9 stabilization. Taken together, tumorigenic ASF1B could be targeted to suppress cervical cancer tumor growth by inducing apoptotic cell death.

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Section: Immunohistochemistrymentioning

confidence: 99%

ASF1B promotes cervical cancer progression through stabilization of CDK9

et al. 2020

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“…In an effort to discover key genes important for PC progression or suppression, we have identified some underinvestigated molecules significantly impacting PC tumorigenesis and metastasis (Qian et al, 2017;Liu et al, 2019). Here, we report another novel finding about LIM domain only 7 (LMO7).…”

Section: Introductionmentioning

confidence: 75%

“…To study the role of LMO7 in PC tumor progression, genetic methods with siRNA, shRNA, and CRISPR-Cas9 technologies were used to establish PC cells with LMO7 knockdown and knockout with our established method (Liu et al, 2019). In this regard, three independent genome-wide siRNAs were designed and transfected to Panc02-H7 cells (Figure 2A).…”

Section: Generation Of Stable Pc Cell Lines With Lmo7 Knockdown and Kmentioning

confidence: 99%

LMO7 as an Unrecognized Factor Promoting Pancreatic Cancer Progression and Metastasis

Liu

Hao

Zhou

et al. 2021

Front. Cell Dev. Biol.

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Pancreatic cancer (PC) is one of the most lethal human malignancies without effective treatment. In an effort to discover key genes and molecular pathways underlying PC growth, we have identified LIM domain only 7 (LMO7) as an under-investigated molecule, which highly expresses in primary and metastatic human and mouse PC with the potential of impacting PC tumorigenesis and metastasis. Using genetic methods with siRNA, shRNA, and CRISPR-Cas9, we have successfully generated stable mouse PC cells with LMO7 knockdown or knockout. Using these cells with loss of LMO7 function, we have demonstrated that intrinsic LMO7 defect significantly suppresses PC cell proliferation, anchorage-free colony formation, and mobility in vitro and slows orthotopic PC tumor growth and metastasis in vivo. Mechanistic studies demonstrated that loss of LMO7 function causes PC cell-cycle arrest and apoptosis. These data indicate that LMO7 functions as an independent and unrecognized druggable factor significantly impacting PC growth and metastasis, which could be harnessed for developing a new targeted therapy for PC.

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“…Of note, previous reports have suggested that the CA17 marker could serve as a potential therapeutic target for hepatocellular carcinoma, 22,37 colorectal, gastric, and pancreatic cancers 43 . In view of the observed high level of CA17 overexpression in CCA, it is tempting to further investigate the therapeutic potential of anti‐CA17 molecules to treat advanced or relapsed CCA patients.…”

Section: Discussionmentioning

confidence: 99%

Clinical correlation of cadherin‐17 marker with advanced tumor stages and poor prognosis of cholangiocarcinoma

Bao

Shen

Wong³

et al. 2021

Journal of Surgical Oncology

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Background and Objectives In this retrospective study, we examined the CA17 tissue expression and analyzed its clinical significance in cholangiocarcinoma (CCA). Materials and Methods Immunohistochemistry was performed to assess CA17 expression on tissue microarrays in a training cohort enrolling 120 CCA patients and a validation cohort comprising 60 CCA patients. Image pro plus was applied to score the staining intensity and expression level of CA17 marker. Kaplan‐Meier analysis, Cox's proportional hazards regression, and nomogram were applied to evaluate the prognostic significance of CA17. Results CA17 cancer biomarker over‐expression was significantly observed in CCA compared to their non‐tumor counterparts, and positively correlated with aggressive tumor phenotypes, like lymph node metastasis. Meanwhile, patients with high expression of CA17 correlated with worse postoperative overall survival (OS) and recurrence‐free survival. Besides, multivariate analysis identified that CA17 expression was an independent prognostic factor for cholangiocarcinoma patients, which indicated that the CA17 could be more efficient than serum CA19‐9 in predicting the OS of CCA patients. Notably, the nomogram integrating CA17 expression had better prognostic performance as compared with current TNM staging systems. Conclusion CA17 was an independent adverse prognostic factor for CCA patients’ survival, which may serve as a promising prognostic biomarker for CCA patients.

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Disruption of oncogenic liver-intestine cadherin (CDH17) drives apoptotic pancreatic cancer death

Cited by 24 publications

References 31 publications

ASF1B promotes cervical cancer progression through stabilization of CDK9

ASF1B promotes cervical cancer progression through stabilization of CDK9

LMO7 as an Unrecognized Factor Promoting Pancreatic Cancer Progression and Metastasis

Clinical correlation of cadherin‐17 marker with advanced tumor stages and poor prognosis of cholangiocarcinoma

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