&lt;p&gt;High Tiam1 expression predicts positive lymphatic metastasis and worse survival in patients with malignant solid tumors: a systematic review and meta-analysis&lt;/p&gt;

Yang, Caixia; Ma, Chenlin; Li, Yingchun; Peng, Mo; Yang, Yusheng

doi:10.2147/ott.s191571

Cited by 5 publications

(5 citation statements)

References 71 publications

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“…Therefore, in PDAC, high level of RASAL2 might cause TIAM1 overexpression. Consistently, TIAM1 acts as a key gene associated with cancer malignancy [30][31][32][33][34], high TIAM1 expression was significantly related with shorter overall survival (OS) and disease-free survival (DFS) and was clearly associated with metastasis in patients with solid cancers [37,38].Our current study has for the first time shown that RASAL2 promotes PDAC malignancy by enhancing YAP1/TIAM1 signaling in PDAC. Specifically, RASAL2 promoted TIAM1 expression by upregulating YAP1.…”

Section: Discussionsupporting

confidence: 67%

“…In PDAC, high expression of TIAM1 suggested a poor prognosis and silencing TIAM1 decreased tumor cell proliferation, migration and invasion [36]. Moreover, a systematic review and meta-analysis revealed that high TIAM1 expression was significantly related with shorter overall survival (OS) and disease-free survival (DFS) and was associated with metastasis in patients with solid cancers [37,38]. PDAC expresses a high level of TIAM1 expression and predicts a poor prognosis, while mechanistically silencing TIAM1 decreases tumor cell proliferation, migration and invasion [36].…”

Section: Discussionmentioning

confidence: 99%

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RASAL2 mediated the enhancement of YAP1/TIAM1 signaling promotes malignant phenotypes of pancreatic ductal adenocarcinoma

Yue¹,

Wu²,

Qian³

et al. 2022

Int. J. Biol. Sci.

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Pancreatic ductal adenocarcinoma (PDAC) is characterized by a high incidence of metastasis and dismal prognosis. As a member of Gas-Gap gene, RASAL2 is involved in the hydrolysis of RAS-GTP to RAS-GDP and abnormal expression in human cancers. Here we firstly described the function of RASAL2 on PDAC to enrich the knowledge of RAS family.We interestingly observed that RASAL2 expression was upregulated in PDAC at both mRNA and protein levels, and high expression of RASAL2 predicted a poor prognosis in PDAC patients. Additionally, RASAL2 promoted malignant behaviors of PDAC in vitro and in vivo. To determine the mechanistic roles of RASAL2 signaling and its potential as a therapeutic target in PDAC, we clarified that RASAL2 could accumulate the TIAM1 expression in different level through inhibiting YAP1 phosphorylation, increased TIAM1 mRNA expression and suppressed ubiquitination of TIAM1 protein. In conclusion, RASAL2 enhances YAP1/TIAM1 signaling and promotes PDAC development and progression.

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Section: Discussionsupporting

confidence: 67%

Section: Discussionmentioning

confidence: 99%

RASAL2 mediated the enhancement of YAP1/TIAM1 signaling promotes malignant phenotypes of pancreatic ductal adenocarcinoma

Yue¹,

Wu²,

Qian³

et al. 2022

Int. J. Biol. Sci.

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“…Tumor-associated lymphatic vessels are closely correlated with metastasis and clinical outcomes in various types of cancer [ [22][23][24]. Herein, the antilymphangiogenic and antilymphatic metastatic functions of aiphanol were explored.…”

Section: Discussionmentioning

confidence: 99%

Aiphanol, a multi-targeting stilbenolignan, potently suppresses mouse lymphangiogenesis and lymphatic metastasis

et al. 2022

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The high incidence of lymphatic metastasis is closely related to poor prognosis and mortality in cancers. Potent inhibitors to prevent pathological lymphangiogenesis and lymphatic spread are urgently needed. The VEGF-C-VEGFR3 pathway plays a vital role in driving lymphangiogenesis and lymph node metastasis. In addition, COX2 in tumor cells and tumor-associated macrophages (TAMs) facilitates lymphangiogenesis. We recently reported that aiphanol, a natural stilbenolignan, attenuates tumor angiogenesis by repressing VEGFR2 and COX2. In this study, we evaluated the antilymphangiogenic and antimetastatic potency of aiphanol using in vitro, ex vivo and in vivo systems. We first demonstrated that aiphanol directly bound to VEGFR3 and blocked its kinase activity with an half-maximal inhibitory concentration (IC 50 ) value of 0.29 μM in an in vitro ADP-Glo TM kinase assay. Furthermore, we showed that aiphanol (7.5−30 μM) dose-dependently counteracted VEGF-C-induced proliferation, migration and tubular formation of lymphatic endothelial cells (LECs), which was further verified in vivo. VEGFR3 knockdown markedly mitigated the inhibitory potency of aiphanol on lymphangiogenesis. In 4T1-luc breast tumor-bearing mice, oral administration of aiphanol (5 and 30 mg• kg −1 •d −1 ) dose-dependently decreased lymphatic metastasis and prolonged survival time, which was associated with impaired lymphangiogenesis, angiogenesis and, interestingly, macrophage infiltration. In addition, we found that aiphanol decreased the COX2-dependent secretion of PGE2 and VEGF-C from tumor cells and macrophages. These results demonstrate that aiphanol is an appealing agent for preventing lymphangiogenesis and lymphatic dissemination by synergistically targeting VEGFR3 and inhibiting the COX2-PGE2-VEGF-C signaling axis.

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“… 71 Furthermore, 1A-116 inhibits Rac1 signalling pathway by preventing its interaction with T-lymphoma invasion and metastasis-inducing protein-1 (TIAM1), a guanine exchange factor, 61 whose high expression is associated with increased lymphatic metastasis and worse patient survival in different cancers. 72 Additionally, 1A-116 has a chronotherapeutic effect against GBM and its efficacy is regulated by the circadian clock. In a study on mouse xenografts (with GBM LN229 cells), Trebucq et al 61 reported that low concentrations of 1A-116 applied near the peak of TIAM1 expression have similar effects for its application with saturating concentrations at different time points.…”

Section: Chronotherapy Drugs/approaches In Glioblastomamentioning

confidence: 99%

Chronotherapy in Glioblastoma: state of the art and future perspectives

Petković¹,

Henis²,

Heese³

et al. 2023

eBioMedicine

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<p>High Tiam1 expression predicts positive lymphatic metastasis and worse survival in patients with malignant solid tumors: a systematic review and meta-analysis</p>

Cited by 5 publications

References 71 publications

RASAL2 mediated the enhancement of YAP1/TIAM1 signaling promotes malignant phenotypes of pancreatic ductal adenocarcinoma

RASAL2 mediated the enhancement of YAP1/TIAM1 signaling promotes malignant phenotypes of pancreatic ductal adenocarcinoma

Aiphanol, a multi-targeting stilbenolignan, potently suppresses mouse lymphangiogenesis and lymphatic metastasis

Chronotherapy in Glioblastoma: state of the art and future perspectives

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