Tanshinone IIA inhibits the proliferation, migration and invasion of ectopic endometrial stromal cells of adenomyosis via 14-3-3ζ downregulation

Wan, Lei; Zou, Yang; Wan, Lihui; Wang, Liqun; Huang, Meizhen; Wu, Juan; Zhu, Yi‐Bao; Huang, Ouping

doi:10.1007/s00404-015-3766-2

Cited by 23 publications

(12 citation statements)

References 40 publications

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“…EESCs (EESC1, EESC2 and EESC3, respectively) were isolated and characterized as described previously (19)(20)(21). In brief, the tissues were washed twice with sterile PBS under aseptic conditions, minced into small pieces, digested by incubation with Dulbecco's modified Eagle's medium (DMEM)/F12 (Hyclone; GE Healthcare Life Sciences, South Logan, UT, USA) supplemented with 1 mg/ml collagenase (Serva Electrophoresis GmbH, Heidelberg, Germany) and 10% fetal bovine serum (FBS; Gibco; Thermo Fisher Scientific, Inc., Waltham, MA, USA) for 2 h at 37˚C and subsequently filtrated with a 70-mm nylon cell strainer.…”

Section: Subjects and Specimensmentioning

confidence: 99%

Berberine inhibits the LPS‑induced proliferation and inflammatory response of stromal cells of adenomyosis tissues mediated by the LPS/TLR4 signaling pathway

et al. 2017

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Abstract.A previous study by our group has demonstrated that lipopolysaccharide (LPS) induces adenomyosis through stimulating inflammatory cell proliferation and invasive growth of stromal cells via Toll-like receptor 4 (TLR4) signaling. The present study aimed to investigate the effects of berberine (BBR) on LPS-induced ectopic endometrial stromal cells (EESCs) isolated from patients with adenomyosis. The viability of EESCs treated with LPS or LPS plus BBR was detected by a cell counting kit-8 assay, and the cell cycle distribution and apoptosis were evaluated by flow cytometry. The effect of BBR on the expression of key molecules of inflammatory proliferation and invasive growth of LPS-induced EESCs was also evaluated. BBR significantly inhibited the LPS-induced proliferation of EESCs in a dose-and time-dependent manner. BBR induced cell cycle arrest in G0/G1 phase and enhanced apoptosis of LPS-induced EESCs. Furthermore, BBR inhibited the expression of interleukin (IL)-6, IL-8, transforming growth factor-β, epithelial growth factor, vascular endothelial growth factor and matrix metalloproteinase 2 in LPS-induced EESCs. To the best of our knowledge, the present study was the first to demonstrate that BBR has a protective effect on ameliorating the LPS-induced progression of adenomyosis. This result may provide a novel therapeutic strategy for the clinical treatment of the disease.

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Section: Subjects and Specimensmentioning

confidence: 99%

Berberine inhibits the LPS‑induced proliferation and inflammatory response of stromal cells of adenomyosis tissues mediated by the LPS/TLR4 signaling pathway

et al. 2017

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“…The primary EESCs were stained positive with anti-vimentin, a specific marker of stromal cells [5, 26], while they were stained negative with anti-cytokeratin by immunocytochemistry, a specific molecular marker for epithelial cells (Figure 1). The purity of isolated EESCs was >95% and cells between passages 4 to 12 were adopted in the current study.…”

Section: Resultsmentioning

confidence: 99%

“…A total of 2 endometrial samples (35- and 42-year-old women) undergoing surgical resection were recruited and the ectopic endometrial tissues were minced into small pieces and incubated with 1 mg/mL type IV collagenase dissolved in complete culture medium for 2 hours at 37°C; the resultant digest was filtrated and centrifuged at 2,000 rpm for 10 minutes; the obtained pellets were collected and grown in complete culture medium, as described previously [5, 25]. The isolated primary EESCs were cultured in DMEM/F12 with 10% FBS, containing 100 IU/mL penicillin and 50 mg/mL streptomycin.…”

Section: Methodsmentioning

confidence: 99%

“…Endometriosis exhibits several features such as aberrant growth and metastasis; the development of this disorder includes a course of cell proliferation, apoptosis, invasion, and migration [4, 5]. Among which, the disrupted balance between cell proliferation and apoptosis are crucial for the development of endometriosis; furthermore, the enhanced cell invasion and migration are also crucial for the development of this disorder [6, 7].…”

Section: Introductionmentioning

confidence: 99%

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Ping‐Chong‐Jiang‐Ni Formula Induces Apoptosis and Inhibits Proliferation of Human Ectopic Endometrial Stromal Cells in Endometriosis via the Activation of JNK Signaling Pathway

Liang

Zou

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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Endometriosis is a common gynecological condition in childbearing age women and its therapy in modern medicine achieves usually temporary cure. Ping-Chong-Jiang-Ni formula (PCJNF), a Chinese herbal medicine (CHM), was shown to be clinically effective on endometriosis. Meanwhile, c-Jun N-terminal kinase (JNK) signaling pathway was involved in the therapeutic process of CHM on endometriosis. Here, we explored the effect of PCJNF on the ectopic endometrial stromal cells (EESCs) from endometriosis and test whether JNK signaling was involved. After being treated with PCJNF-containing serum obtained from Sprague Dawley rat, cell proliferation, migration, invasion, and apoptosis were evaluated in EESCs, and the total and phosphorylated JNK, ERK, and p38 proteins were detected. Our results showed that PCJNF could suppress cell proliferation, migration, and invasion and induce apoptosis in EESCs. The suppressed proliferation and increased apoptosis were dependent on JNK activation. Additionally, PCJNF caused cell cycle arrest at G2/M phase and this effect was mediated by JNK signaling, while the decreased cell migration and invasion treated by PCJNF were independent of JNK signaling. In summary, our results provided the first evidence that PCJNF could suppress cell proliferation, migration, and invasion, while increasing apoptosis in EESCs, and the suppressed proliferation and enhanced apoptosis were mediated by JNK signaling.

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“…Prior study showed that 14-3-3ζ impaired cell proliferation in human ectopic endometrial in vitro [21]. 14-3-3ζ dysregulates BH3-only protein and leads to a lower level of Bax activation resulting in apoptosis suppression [22–23].…”

Section: Discussionmentioning

confidence: 99%

14-3-3ζ/TGFβR1 promotes tumor metastasis in lung squamous cell carcinoma

et al. 2016

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14-3-3ζ is involved in tumor cell growth and apoptosis. However, the mechanism of 14-3-3ζ in lung squamous cell carcinoma (SCC) metastasis has not been illuminated. In our studies, we found that the expression of 14-3-3ζ was highly expressed in lung SCC compared to normal lung tissues. High expression of 14-3-3ζ was associated with pTNM stage (p<0.05) and lymph node metastasis (p<0.05). Furthermore, the expression of 14-3-3ζ protein was associated with high levels of TGFβR1 protein (p=0.005), and pSMAD3 (p=0.033). Lung SCC patients with high 14-3-3ζ expression have significantly shorter OS and DFS compared to patients with low 14-3-3ζ expression. Additionally, 14-3-3ζ knockdown inhibited cell proliferation, migratory and invasive properties of human lung SCC cells. TGFβR1 was involved in 14-3-3ζ-mediated cell proliferation and metastasis of lung SCC cells. Additionally, sh-14-3-3ζ can suppress tumor growth and metastasis in vivo. Thus, these data provide the evidence that 14-3-3ζ promote tumor metastasis and might be a prognostic biomarker and target for therapeutic strategy in lung SCC.

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Tanshinone IIA inhibits the proliferation, migration and invasion of ectopic endometrial stromal cells of adenomyosis via 14-3-3ζ downregulation

Cited by 23 publications

References 40 publications

Berberine inhibits the LPS‑induced proliferation and inflammatory response of stromal cells of adenomyosis tissues mediated by the LPS/TLR4 signaling pathway

Berberine inhibits the LPS‑induced proliferation and inflammatory response of stromal cells of adenomyosis tissues mediated by the LPS/TLR4 signaling pathway

Ping‐Chong‐Jiang‐Ni Formula Induces Apoptosis and Inhibits Proliferation of Human Ectopic Endometrial Stromal Cells in Endometriosis via the Activation of JNK Signaling Pathway

14-3-3ζ/TGFβR1 promotes tumor metastasis in lung squamous cell carcinoma

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