CRKL knockdown promotes in vitro proliferation, migration and invasion, in vivo tumor malignancy and lymph node metastasis of murine hepatocarcinoma Hca-P cells

Meng, Lingyu; Sun, Ming‐Zhong; Guo, Chunmei; Sun, Xujuan; Lin, Qiu-Yue; Liu, Shuqing

doi:10.1016/j.biopha.2015.02.022

Cited by 15 publications

(21 citation statements)

References 39 publications

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“…and invasion, and in vivo tumor malignancy and LNM rate levels of Hca-P cells (22,23). In the present study, the potential tumor promoter role of CRKII in hepatocarcinoma was investigated.…”

Section: Crkii Overexpression Promotes the In Vitro Proliferation MImentioning

confidence: 91%

“…Hca-P and Hca-F are two mouse hepatocarcinoma ascites cell lines sharing the same genetic background (15,(22)(23)(24). Hca-F has a high LNM rate of 75% and Hca-P has a low LNM metastasis rate of 25%.…”

Section: Introductionmentioning

confidence: 99%

“…They metastasize only to lymph nodes, and do not disseminate to other organs (25). Hca-P cell is used as a low-LNM and LN-specific murine hepatocarcinoma cell model for the early discovery and diagnosis of tumor malignancies (15,(22)(23)(24)(25). Our previous study indicated that CRK is involved in the lymphatic metastatic potential of murine hepatocarcinoma cells (22,23).…”

Section: Introductionmentioning

confidence: 99%

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CRKII overexpression promotes the in�vitro proliferation, migration and invasion potential of murine hepatocarcinoma Hca‑P cells

et al. 2019

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Section: Crkii Overexpression Promotes the In Vitro Proliferation MImentioning

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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CRKII overexpression promotes the in�vitro proliferation, migration and invasion potential of murine hepatocarcinoma Hca‑P cells

et al. 2019

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“…Its dysexpression is linked to the development, metastasis and drug-resistance of various cancers. Previous work from our lab using a pair of syngenetic murine hepatocarcinoma ascites cell lines, Hca-F with 75% and Hca-P with 25% LNM rates [10][11][12][13][14], indicated ANXA5 was a potential promoter in murine hepatocarcinoma tumorigenicity and lymphatic metastasis. ANXA5 upregulation enhanced the tumorigenicity, LNM rate and level of Hca-P-transplanted mice [7,14].…”

Section: Introductionmentioning

confidence: 92%

ANXA5 Enhances Malignancy of Murine Hepatocarcinoma Hca-P Cells <i>via</i> ERK Activation and E-cadherin Suppression

Liu¹

2019

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The invasion and metastasis are linked to the rapid progression and poor prognosis of hepatocarcinoma patients.Lymphatic metastasis is potentially involved in above pathogenesis with unclear mechanism. Previously, we found the deregulation of annexin A5 (ANXA5), a member of Ca 2+ -regulated phospholipid-and membrane-binding annexin family protein, mediated the in vivo malignancy, lymph node metastasis (LNM) rate and level of mice transplanted with Hca-P, a murine hepatocarcinoma cell line with the LNM potential rate of ~25%. Current work aimed to investigate the influence with action mechanism of ANXA5 overexpression on the in vitro malignant behaviours of Hca-P cells. For overexpressing ANXA5, the Anxa5 gene was ligated into pCDNA3.1 (+) vector and transfected into Hca-P named as Hca-P-ANXA5up. Hca-P transfected with empty pCDNA3.1 (+) vector was named as Hca-P-mock and used as the control. The monoclonal Hca-P-mock and Hca-P-ANXA5up cell lines were obtained against G418 screening using limiting dilution method. Compared with the Hca-P-mock cells, Western blotting assay indicated ANXA5 expression level was increased by 50.1% (p=0.025) in the Hca-P-ANXA5up cells. Transwell chamber assays indicated that the migration and invasion capacities of Hca-P-ANXA5up cells were increased by 150.2% (p=0.001) and 94.8% (p=0.003) than Hca-P-mock cells. ANXA5 overexpression enhanced the levels of p-MEK (Ser217/221), ERK1, ERK2, p-ERK1 (Thr202/Tyr204) and p-ERK2 (Thr185/Tyr187), and suppressed the levels of E-Cadherin, Snail and Slug in Hca-P cells. Current work shows ANXA5 overexpression enhances the malignant behaviours of hepatocarcinoma Hca-P cells through activating p-MEK-ERK pathway and suppressing E-Cadherin, Snail and Slug. It is of potential value in tumor malignancy and lymphatic metastasis of hepatocarcinoma.

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“…A number of protein substrates of Abl’s tyrosine kinase activity have been reported previously 1 . One of these is the protein CrkL, an SH2/SH3 domain adaptor protein, which upon tyrosine phosphorylation can stimulate multiple signaling pathways that drive cell proliferation and invasion 5 .…”

Section: Introductionmentioning

confidence: 99%

Analysis of Cellular Tyrosine Phosphorylation via Chemical Rescue of Conditionally Active Abl Kinase

et al. 2018

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Identifying direct substrates targeted by protein kinases is important in understanding cellular physiology and intracellular signal transduction. Mass-spectrometry based quantitative proteomics provides a powerful tool for comprehensively characterizing the downstream substrates of protein kinases. This approach is efficiently applied to receptor kinases which can be precisely, directly, and rapidly activated by some agent, such as a growth factor. However, non-receptor tyrosine kinase Abl lacks the experimental advantage of extracellular growth factors as immediate and direct stimuli. To circumvent this limitation, we combine a chemical rescue approach with quantitative phosphoproteomics to identify targets of Abl and their phosphorylation sites with enhanced temporal resolution. Both known and novel putative substrates are identified, presenting opportunities for studying unanticipated functions of Abl under physiological and pathological conditions.

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CRKL knockdown promotes in vitro proliferation, migration and invasion, in vivo tumor malignancy and lymph node metastasis of murine hepatocarcinoma Hca-P cells

Cited by 15 publications

References 39 publications

CRKII overexpression promotes the in�vitro proliferation, migration and invasion potential of murine hepatocarcinoma Hca‑P cells

CRKII overexpression promotes the in�vitro proliferation, migration and invasion potential of murine hepatocarcinoma Hca‑P cells

ANXA5 Enhances Malignancy of Murine Hepatocarcinoma Hca-P Cells <i>via</i> ERK Activation and E-cadherin Suppression

Analysis of Cellular Tyrosine Phosphorylation via Chemical Rescue of Conditionally Active Abl Kinase

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CRKL knockdown promotes in vitro proliferation, migration and invasion, in vivo tumor malignancy and lymph node metastasis of murine hepatocarcinoma Hca-P cells

Cited by 15 publications

References 39 publications

CRKII overexpression promotes the in�vitro proliferation, migration and invasion potential of murine hepatocarcinoma Hca‑P cells

CRKII overexpression promotes the in�vitro proliferation, migration and invasion potential of murine hepatocarcinoma Hca‑P cells

ANXA5 Enhances Malignancy of Murine Hepatocarcinoma Hca-P Cells &lt;i&gt;via&lt;/i&gt; ERK Activation and E-cadherin Suppression

Analysis of Cellular Tyrosine Phosphorylation via Chemical Rescue of Conditionally Active Abl Kinase

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ANXA5 Enhances Malignancy of Murine Hepatocarcinoma Hca-P Cells <i>via</i> ERK Activation and E-cadherin Suppression