Semaphorin3F Down-Regulates the Expression of Integrin α&lt;sub&gt;v&lt;/sub&gt;β&lt;sub&gt;3&lt;/sub&gt; and Sensitizes Multicellular Tumor Spheroids to Chemotherapy via the Neuropilin-2 Receptor in vitro

Zheng, Chenhong; Zhou, Qi; Wu, Feng; Peng, Qiyu; Tang, Airong; Liang, Houjie; Zeng, Yanjun

doi:10.1159/000232449

Cited by 15 publications

(22 citation statements)

References 55 publications

(43 reference statements)

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“…Since U251MG cells have NRP2, the receptor for SEMA 3G and SEMA 3F, and SEMA3F blocked tumor formation by associating with loss of activated αvβ3 integrin, impaired cell adhesion to extracellular matrix components (36,41,42), it could be informative to determine the mechanism of SEMA3G in tumorigenesis and invasive progression.…”

Section: Discussionmentioning

confidence: 99%

Effects of SEMA3G on migration and invasion of glioma cells

Zhou

et al. 2012

Oncol Rep

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Abstract. Glioblastoma multiforme is the most aggressive type of brain tumor with a strong ability to invade and migrate into surrounding normal brain tissues, leading to high tumor recurrence and mortality. Most of class-3 semaphorins, especially SEMA3A, SEMA3B and SEMA3F, have been reported to have strong tumor inhibition ability, but the role of SEMA3G in tumor biology is largely unknown. We report here that SEMA3G possesses anti-migration and anti-invasion ability. To determine the potential effects of SEMA3G on migratory and invasive ability, we generated stable SEMA3G expression U251MG cells. We found that stably overexpressed SEMA3G inhibited the migratory and invasive behavior of U251MG cells. In addition, treatment with SEMA3G conditioned media also decreased the migratory and invasive ability of parental U251MG cells. Furthermore, SEMA3G also inhibited the activity of MMP2, an index of tumor invasion ability. Thus, our results suggest that SEMA3G inhibited tumor cell migration and invasion, which may be obtained through cell autonomous or paracrine mechanisms, and SEMA3G is a potential target for antitumor migration and invasion.

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Section: Discussionmentioning

confidence: 99%

Effects of SEMA3G on migration and invasion of glioma cells

Zhou

et al. 2012

Oncol Rep

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“…Previous studies also showed that the most common tumor suppressor gene of endometrioid carcinoma, PTEN, is involved in the interaction of PINCH-ILK by the Pi3 kinase pathway [26] . Thus, the role of PINCH as a crucial adapter protein between integrin and growth factor signal transduction pathways, like other molecular targeted agents, merits further study in the treatment of endometrial cancer and other common malignant tumors after surgical resection, hormonal therapy, radiation and chemotherapy [27][28][29] .…”

Section: Discussionmentioning

confidence: 99%

PINCH Protein Expression in Normal Endometrium, Atypical Endometrial Hyperplasia and Endometrioid Endometrial Carcinoma

Zhang¹,

Li²,

Zhang³

et al. 2010

Chemotherapy

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Background: Particularly interesting new cysteine-histidine rich protein (PINCH), as an adapter protein of the LIM family for signal transduction in the integrin and growth factor pathway, is upregulated in the stroma of several common types of cancers and involved in promoting tumor progression. In the present study, we examined PINCH expression in normal endometrium, atypical endometrial hyperplasia and endometrioid carcinoma, and further studied the relationships of PINCH expression with clinicopathological variables in cancer patients. Methods: PINCH expression was examined by immunohistochemistry in 23 normal endometrial samples, 18 atypical endometrial hyperplasias and 48 endometrioid endometrial carcinomas. Results: The PINCH expression in the stroma of cancer (71%) was significantly increased compared to either normal endometrium (17%, p < 0.0001) or atypical hyperplasia (39%, p = 0.017), along with 9 cancers that had stronger PINCH expressions at the invasive margin of the cancers compared to the inner cancers. PINCH expression in cancer was higher in the patients with hypertension (p = 0.041) and estrogen exposure time >30 years (p = 0.021). On the other hand, PINCH expression was not related to menopausal status, gravid status, blood sugar/lipid, family background of cancer, histological grade, myometrial invasion, cervical involvement, lymph nodal metastases, growth pattern, estrogen and progestogen receptors (p > 0.05). Conclusion: The results suggest that PINCH seems to play a role, presently unknown, in the tumorigenesis and development of endometrial cancer that merits further study.

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“…Several class 3 SEMAs, including SEMA3A, SEMA3B, SEMA3E and SEMA3F, have been characterized as anti-angiogenic agents (14)(15)(16)(17)(18)(19). For example, SEMA3B, SEMA3F and SEMA4D regulate tumor angiogenesis, growth and metastasis in different manners (20,21). Previous studies showed that SEMA3A, which is considered as the candidate tumor suppressor, is often downregulated in numerous types of cancer, including…”

Section: Introductionmentioning

confidence: 99%

Decreased semaphorin 3A expression is associated with a poor prognosis in patients with epithelial ovarian carcinoma

Jiang

Wang

et al. 2015

International Journal of Molecular Medicine

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Semaphorin 3A (SEMA3A) was initially identified to play an important role in axonal guidance. Recently, SEMA3A has also been considered as a candidate tumor suppressor, since it is often downregulated in numerous types of cancer, including prostate cancer, breast cancer and glioma. However, the biological role of SEMA3A in ovarian cancer is not clear. In the present study, the expression of SEMA3A in ovarian cancer and normal ovarian epithelial tissues was detected by immunofluorescence, reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blotting, and the associations between the expression of SEMA3A with the development of ovarian cancer, clinicopathological characteristics and survival were also analyzed. Results from immunofluorescence, RT‑qPCR and western blotting showed that SEMA3A is significantly downregulated in epithelial ovarian carcinoma compared to normal ovarian epithelial specimens (P<0.05). The expression levels of SEMA3A were lower in the cancer tissues with III/IV stage [the International Federation of Gynecology and Obstetrics (FIGO) stage], poor histological grade, lymph node metastasis and distant metastasis compared to that in the cancer tissues with I/II stage (FIGO), well histological grade, or without lymph node metastasis and distant metastasis (P<0.05). A decreased expression of SEMA3A is associated with a poor prognosis (P<0.001). The present findings suggest that decreased SEMA3A expression may be associated with the development of epithelial ovarian carcinoma, and therefore, SEMA3A may be a valuable prognostic marker, as well as a potential molecular therapy target for ovarian cancer patients.

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Semaphorin3F Down-Regulates the Expression of Integrin α<sub>v</sub>β<sub>3</sub> and Sensitizes Multicellular Tumor Spheroids to Chemotherapy via the Neuropilin-2 Receptor in vitro

Cited by 15 publications

References 55 publications

Effects of SEMA3G on migration and invasion of glioma cells

Effects of SEMA3G on migration and invasion of glioma cells

PINCH Protein Expression in Normal Endometrium, Atypical Endometrial Hyperplasia and Endometrioid Endometrial Carcinoma

Decreased semaphorin 3A expression is associated with a poor prognosis in patients with epithelial ovarian carcinoma

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