Regulation of estrogen receptor α function in oral squamous cell carcinoma cells by FAK signaling

Chang, Yi-Lin; Hsu, Yu-Kan; Wu, Tsung-Fan; Huang, Chenn‐Jung; Liou, Li-Yin; Chiu, Yu‐Han; Hsiao, Yu-Hsuan; Luo, Fuh-Jinn; Yuan, Ta‐Chun

doi:10.1530/erc-14-0102

Cited by 30 publications

(34 citation statements)

References 43 publications

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“…The treatment with tamoxifen significantly inhibits OSCC cell proliferation and invasion (14,15,21-23). Therefore, the usage of tamoxifen for targeted therapies may be useful for hormonally active OSCCs.…”

Section: Discussionmentioning

confidence: 99%

Estrogen and Progesterone hormone receptor expression in oral cavity cancer

Grimm

Biegner²,

Teriete³

et al. 2016

Med Oral

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BackgroundRecent studies have shown an increase in the incidence of oral squamous cell carcinoma (OSCC) in younger patients. The hypothesis that tumors could be hormonally induced during pregnancy or in young female patients without the well-known risk factors alcohol or tobacco abuse seems to be plausible.Material and MethodsEstrogen Receptor alpha (ERα) and Progesterone Receptor (PR) expression were analyzed in normal oral mucosa (n=5), oral precursor lesions (simple hyperplasia, n=11; squamous intraepithelial neoplasia, SIN I-III, n=35), and OSCC specimen. OSCCs were stratified in a young female (n=7) study cohort and older patients (n=46). In the young female study cohort three patients (n=3/7) developed OSCC during or shortly after pregnancy. Breast cancer tissues were used as positive control for ERα and PR expression.ResultsERα expression was found in four oral precursor lesions (squamous intraepithelial neoplasia, SIN I-III, n=4/35, 11%) and in five OSCC specimen (n=5/46, 11%). The five ERα positive OSCC samples were older male patients. All patients within the young female study cohort were negatively stained for both ERα and PR.ConclusionsER expression could be regarded as a seldom risk factor for OSCC. PR expression seems to be not relevant for the development of OSCC. Key words:Oral squamous cell carcinoma, estrogen receptor, progesterone receptor, hormone receptor.

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Section: Discussionmentioning

confidence: 99%

Estrogen and Progesterone hormone receptor expression in oral cavity cancer

Grimm

Biegner²,

Teriete³

et al. 2016

Med Oral

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“…19 For expressing FAK proteins in SCC4 or OECM-1 cells, 293FT cells (Invitrogen) were cotransfected with the pCDH vector containing the wild-type or Y397F FAK cDNAs plus packaging plasmids, using PolyJet Transfection Reagent (SignaGen Laboratories, Ijamsville, MD, USA). The control cells were cotransfected with the pCDH vector alone plus packaging plasmids.…”

Section: Lentiviral Infectionmentioning

confidence: 99%

“…The procedure of immunohistochemical staining has been described previously. 19 Briefly, the sections were deparaffinized in xylene, rehydrated with graded ethanol, and then boiled in 1 mM EDTA (pH 8.0) for 5 min in an autoclave. After three washes with 3% H 2 O 2 , the sections were blocked with a protein block serum (Dako Glostrup, Denmark) for 5 min.…”

Section: Tissue Microarray and Immunohistochemistrymentioning

confidence: 99%

“…We next compared the motility and invasiveness of SCC4 and OECM-1 cells. Because the growth rate of OECM-1 cells is much higher than that of SCC4 cells, 19 we performed the migration and invasion assays in the presence of hydroxyurea, a cell cycle blocker, in order to eliminate any effect caused by differential growth properties. As shown in Figure 2b, the number of migrated or invaded OECM-1 cells was ∼ 3-10 fold higher than those in SCC4 cells (Po0.01).…”

Section: Fak Expression and Py397 Correlates With The Activities Of Rmentioning

confidence: 99%

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Tyrosine 397 phosphorylation is critical for FAK-promoted Rac1 activation and invasive properties in oral squamous cell carcinoma cells

Yuan

2016

Laboratory Investigation

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Oral squamous cell carcinoma (OSCC) is a common cancer worldwide. Despite advances in diagnosis and therapy, treatment options for patients with metastatic OSCC are few, due in part to the limited understanding of the molecular events involved in the invasion and metastasis of OSCC. In this study, we investigated the expression of focal adhesion kinase (FAK) and its tyrosine 397 phosphorylation (pY397) in the tissue specimens of OSCC. The roles of pY397 in regulating the activities of Rac1 and cortactin and the invasive properties of OSCC cells were further determined. Results from immunohistochemical analyses in 9 benign, 19 premalignant, and 19 malignant oral tissues showed that the immunoreactivity of FAK was observed in 5 benign (56%), 19 premalignant (100%), and 18 malignant tissues (95%), whereas the immunoreactivity of pY397 was only found in 1 of 9 (11%) benign lesions but was observed in 9 premalignant (47%) and 12 malignant (63%) lesions. Compared with the low-invading SCC4 cells, the high-invading OECM-1 cells exhibited higher levels of FAK expression and pY397, correlating with higher levels of GTP-bound Rac1 and cortactin phosphorylation. Manipulation of FAK expression or Y397 phosphorylation in SCC4, FaDu, OECM-1, or HSC-3 cells regulated their Rac1 activities and invasive properties. Furthermore, treatment of NSC23766, a Rac1-specific inhibitor, in OECM-1 and HSC-3 cells led to reduced invasive properties. Nevertheless, knockdown of FAK expression or suppression of pY397 had no effect on the cortactin activity in OECM-1 cells. The data collectively suggest that pY397 plays critical roles in the FAK-promoted Rac1 activation and invasive properties in OSCC cells. Thus, the inhibition of FAK phosphorylation at Y397 or Rac1 activity can serve as a therapeutic strategy for treating patients with metastatic OSCC. Oral squamous cell carcinoma (OSCC) is the most common malignancy occurring in the oral cavity that usually arises from the buccal mucosa and tongue. During the tumor progression, OSCC cells gradually spread and invade to neighboring tissues, including the nasal cavity or the maxillary facial structures, and eventually metastasize to neck lymph nodes and distant organs. 1 Similar to other malignant diseases, tumor metastasis is a great challenge for the treatment of OSCC. This notion is supported by the fact that only 50% of diagnosed OSCC patients can survive for 5 years, and this is mainly because OSCC patients continue to die from tumor relapse at regional or distant sites. 2 Despite advances in diagnosis and therapy in past decades, the promising strategy for treating patients with metastatic OSCC is still underdeveloped, due in part to the limited understanding of the molecular events involved in invasion and metastasis of OSCC. The underlying molecular basis of OSCC metastasis deserves intensive study.Focal adhesion kinase (FAK) is a nonreceptor tyrosine kinase and functionally involves the regulatory processes of multiple cellular events, including adhesion, migration, invasion, prolifer...

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“…Cells were harvested, and the cell lysates were prepared as described previously (Chang et al 2014). For immunoblotting, an aliquot of total cell lysates in an SDS-PAGE sample buffer was separated by 23:8 electrophoresis and then transferred to a nitrocellulose membrane.…”

Section: Cell Lysis and Immunoblottingmentioning

confidence: 99%

PYK2 via S6K1 regulates the function of androgen receptors and the growth of prostate cancer cells

Hsiao¹,

Huang²,

Hung³

et al. 2016

Endocrine-Related Cancer

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Androgen receptor (AR) is a steroid hormone receptor that functions as a transcription factor for regulating cell growth and survival. Aberrant AR function becomes a risk factor for promoting the progression of prostate cancer (PCa). In this study, we examined the roles of proline-rich tyrosine kinase 2 (PYK2) and ribosomal S6 kinase 1 (S6K1) in regulating AR expression and activity and growth properties in PCa cells. Compared with normal prostate tissues, PCa tumors exhibited high levels of PYK2 and S6K1 expression. Furthermore, the expression levels of PYK2 and S6K1 were significantly correlated with nuclear AR expression in PCa tissues. We further found the association between PYK2, S6K1, and AR in their protein expression and phosphorylation levels among normal prostate PZ-HPV-7 cells and prostate cancer LNCaP and 22Rv1 cells. Overexpression of the wild-type PYK2 in PZ-HPV-7 and LNCaP cells promoted AR and S6K1 expression and phosphorylation as well as enhanced cell growth. In contrast, expression of the mutated PYK2 or knockdown of PYK2 expression in LNCaP or 22Rv1 cells caused reduced expression or phosphorylation of AR and S6K1 as well as retarded cell growth. Under an androgen-deprived condition, PYK2-promoted AR expression and phosphorylation and PSA production in LNCaP cells can be abolished by knocking down S6K1 expression. In summary, our data suggested that PYK2 via S6K1 activation modulated AR function and growth properties in PCa cells. Thus, PYK2 and S6K1 may potentially serve as therapeutic targets for PCa treatment.

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Regulation of estrogen receptor α function in oral squamous cell carcinoma cells by FAK signaling

Cited by 30 publications

References 43 publications

Estrogen and Progesterone hormone receptor expression in oral cavity cancer

Estrogen and Progesterone hormone receptor expression in oral cavity cancer

Tyrosine 397 phosphorylation is critical for FAK-promoted Rac1 activation and invasive properties in oral squamous cell carcinoma cells

PYK2 via S6K1 regulates the function of androgen receptors and the growth of prostate cancer cells

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