Involvement of <scp>ER</scp>‐α36 in the malignant growth of gastric carcinoma cells is associated with <scp>GRP</scp>94 overexpression

Fu, Zhengqi; Deng, Hao; Wang, Xüming; Yang, Xinyi; Wang, Zhaoyi; Liu, Lijiang

doi:10.1111/his.12171

Cited by 21 publications

(28 citation statements)

References 31 publications

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“…In ER-α36-knockdown SGC-7901 cells, downregulated ER-α36 expression was associated with smaller tumor size, decreased nuclear fission and reduced GRP94 expression (25). In the present study, a high level of ER-α36 expression was detected in specimens from patients with gastric carcinoma, which was positively associated with GRP78 expression.…”

Section: Discussionsupporting

confidence: 61%

“…The ER-α36-specific shRNA expression vector was constr ucted by cloning the DNA oligonucleotides (5'-TTA AC CGT ACC ACT CTG CTG ATT GAT ATC CGT CAG CAG AGT GGT ACG GTT A-3') targeting the 3'-untranslated region of ER-α36 cDNA into the pRNAT-U6.1/neo expression vector purchased from GenScript Biotech Corporation (Piscataway, NJ, USA). A gastric cancer cell line overexpressing ER-α36 (SGC-7901-High36 cells) was established via transfection with an ER-α36 expression vector, as previously described (11,13,25,29). SGC-7901, SGC-7901-Low36 cells and SGC-7901-High36 were all maintained in RPMI-1640 medium (Gibco; Thermo Fisher Scientific, Inc.) with 10% fetal bovine serum (FBS; Gibco; Thermo Fisher Scientific, Inc.) at 37˚C in an atmosphere containing 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

“…Prior to E2 treatment, cells were cultured at 37˚C in phenol-red-free medium (Gibco; Thermo Fisher Scientific, Inc.) with 5% charcoal-stripped FBS (Biological Industries, Kibbutz Beit-Haemek, Israel) for 6 h, and then in 2% charcoal-stripped FBS for 24 h, then cells were treated with 10 -10 M E2 for 24 h. Western blot analysis. Western blot analysis was conducted as previously described (25). Briefly, cells were washed with cold PBS and lysed with RIPA buffer.…”

Section: Methodsmentioning

confidence: 99%

“…The immunostained slides were evaluated independently by two pathologists in a double-blinded manner. In the majority of cases, the evaluations of the two pathologists were identical; discrepancies were resolved by re-examination and consensus (25).…”

Section: Grp78 Expression ---------------------------------------mentioning

confidence: 99%

“…GRP78 overexpression was detected in samples from aggressive ER-negative breast cancer, but not in those from benign human breast lesions (24). Elevated GRP94 expression was also reported to be associated with cancer progression and ER-α36 expression in gastric and breast cancer (25,26). Crosstalk between GRP94, ER-α36 and HER2 forms positive feedback loops in breast cancer, which may affect tumor growth, metastasis and drug resistance (26).…”

Section: Introductionmentioning

confidence: 99%

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Estrogen receptor‑α36‑mediated rapid estrogen signaling regulates 78 kDa glucose‑regulated protein expression in gastric carcinoma cells

Wang

et al. 2018

Oncol Lett

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Abstract.To determine whether estrogen receptor-α36 (ER-α36) -mediated rapid estrogen signaling is associated with 78 kDa glucose-regulated protein (GRP78) expression in gastric cancer, 86 samples of gastric tumor tissue with corresponding normal and tumor-adjacent tissues were used to examine expression patterns of GRP78 and ER-α36. Immunohistochemistry demonstrated that 55/86 (63.95%) patients with gastric carcinoma, and western blot analysis revealed that GRP78 was upregulated in 15/20 (75%) of tumor specimens. GRP78 expression was positively associated with ER-α36 expression, the male sex and lymph node metastasis (P<0.05). Estrogen treatment increased GRP78 and ER-α36 expression, as well as GSK-3β phosphorylation in established gastric cancer SGC-7901 cells. The steady-state level of GRP78 protein expression and the level of phosphorylated GSK-3β at Ser9 were decreased in SGC-7901 cells with ER-α36 knockdown. Forced expression of ER-α36 in SGC-7901 cells, however, led to an increase in GRP78 expression and GSK-3β phosphorylation. It may therefore be concluded that ER-α36-mediated rapid estrogen signaling positively regulates GRP78 expression, presumably via the GSK-3β pathway, which may be associated with gastric carcinogenesis.

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Section: Discussionsupporting

confidence: 61%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Grp78 Expression ---------------------------------------mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Estrogen receptor‑α36‑mediated rapid estrogen signaling regulates 78 kDa glucose‑regulated protein expression in gastric carcinoma cells

Wang

et al. 2018

Oncol Lett

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Knockdown of ER‐α36 expression inhibits glioma proliferation, invasion and epithelial‐to‐mesenchymal transition

Zhao

Xiang

Yang

et al. 2021

The Anatomical Record

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Estrogen receptor-α36 (ER-α36), a subtype of the estrogen receptor, is reported to play roles in tumorigenesis and tamoxifen resistance in several tumors, especially breast cancer. However, the role of ER-α36 in glioma proliferation and invasion remains unknown. Here, we explored the function of ER-α36 in glioma cells, using U87 and U251 cell lines. We found that ER-α36 was upregulated in glioma tissues compared to adjacent nontumor tissues. In U87 and U251 glioma cell lines, inhibition of ER-α36 expression by shRNA suppressed cell proliferation and invasion. In addition, the expression of an epithelial marker, ZO-1, was upregulated while that of one mesenchymal marker, N-cadherin, was downregulated with ER-α36 knockdown.We also found that inhibition of ER-α36 inactivated both PI3K/AKT and MEK/ERK signals. Taken together, these data indicated that overexpression of ER-α36 is associated with glioma proliferation and progression but that inhibition of ER-α36 leads to suppressed invasion and the epithelial-tomesenchymal transition via PI3K/AKT and MEK/ERK pathway inactivation in glioma cells.

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The biology and inhibition of glucose‐regulated protein 94/gp96

Pugh

Alnaed

Brackett

et al. 2022

Medicinal Research Reviews

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The 94 kDa molecular chaperone, glucose-regulated protein 94 (Grp94), has garnered interest during the last decade due to its direct association with endoplasmic reticulum (ER) stress and disease. Grp94 belongs to the Hsp90 family of molecular chaperones and is a master regulator of ER homeostasis due to its ability to fold and stabilize proteins/receptors, and to chaperone misfolded proteins for degradation. Multiple studies have demonstrated that Grp94 knockdown or inhibition leads to the degradation of client protein substrates, which leads to disruption of disease-dependent signaling pathways. As a result, small molecule inhibitors of Grp94 have become a promising therapeutic approach to target a variety of disease states. Specifically, Grp94 has proven to be a promising target for cancer, glaucoma, immune-mediated inflammation, and viral infection. Moreover, Grp94-peptide complexes have been utilized effectively as adjuvants for vaccines against a variety of disease states. This work highlights the significance of Grp94 biology and the development of therapeutics that target this molecular chaperone in multiple disease states.

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Involvement of ER‐α36 in the malignant growth of gastric carcinoma cells is associated with GRP94 overexpression

Abstract: Glucose-regulated protein 94 is a downstream effector of ER-α36-mediated oestrogen signalling, and may be involved in ER-α36 function during gastric carcinogenesis.

Cited by 21 publications

References 31 publications

Estrogen receptor‑α36‑mediated rapid estrogen signaling regulates 78 kDa glucose‑regulated protein expression in gastric carcinoma cells

Estrogen receptor‑α36‑mediated rapid estrogen signaling regulates 78 kDa glucose‑regulated protein expression in gastric carcinoma cells

Knockdown of ER‐α36 expression inhibits glioma proliferation, invasion and epithelial‐to‐mesenchymal transition

The biology and inhibition of glucose‐regulated protein 94/gp96

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