TRPP2 Enhances Metastasis by Regulating Epithelial-Mesenchymal Transition in Laryngeal Squamous Cell Carcinoma

Wu, Kaile; Shen, Bing; Jiang, Feifei; Xia, Lin; Fan, Taotao; Qin, Maolin; Yang, Lei; Guo, Jizheng; Li, Yifan; Zhu, Min; Du, Juan; Liu, Yehai

doi:10.1159/000447914

Cited by 36 publications

(36 citation statements)

References 38 publications

(52 reference statements)

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“…Emerging evidence suggests that epithelial-mesenchymal transition (EMT), which is an essential phenotypic conversion during embryonic development, tissue remodeling, and wound healing, plays an important role in cancer metastasis [2][3][4]. During EMT, epithelial cells acquire fibroblast-like properties, exhibit reduced intercellular adhesion, and show increased motility.…”

Section: Introductionmentioning

confidence: 99%

Stabilization of Slug by NF-κB is Essential for TNF-α -Induced Migration and Epithelial-Mesenchymal Transition in Head and Neck Squamous Cell Carcinoma Cells

Liu

Shi

Wang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Slug protein, a transcription factor for the induction of epithelial-mesenchymal transition (EMT) and cancer cell invasion and metastasis, is frequently upregulated in human epithelial cancers. However, mutation of this gene in cancer is rare, and the mechanism of its dysregulation remains unknown, especially in head and neck squamous cell carcinoma (HNSCC). Methods: We examined the role of TNF-α in the stabilization of Slug by immunoprecipitation-westernblot analysis. Migration of HNSCC cells with or without knockdown of Slug gene expression was assayed by a wound healing assay. Immunohistochemical staining analysis was used to measurement Slug levels in both normal and HNSCC tumor tissues. Results: The inflammatory cytokine TNF-α stabilized Slug protein by inhibiting its ubiquitination through the NF-κB pathway. Inhibition of NF-κB or knockdown of p65 abrogated the TNF-α-induced stabilization of Slug. Knockdown of Slug expression inhibited cancer cell migration and EMT characteristics induced by TNF-α. Moreover, increased levels of Slug were found to correlate with lymph node metastasis and predict poor prognosis in patients with HNSCC. Conclusions: NF-κB-mediated stabilization of Slug underlies the inflammation-induced EMT and metastasis in HNSCC, which may serve as a therapeutic target for metastatic HNSCC.

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Section: Introductionmentioning

confidence: 99%

Stabilization of Slug by NF-κB is Essential for TNF-α -Induced Migration and Epithelial-Mesenchymal Transition in Head and Neck Squamous Cell Carcinoma Cells

Liu

Shi

Wang

et al. 2018

Cell Physiol Biochem

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“…For example, Snail and Slug can bind to E-cadherin promoter and repress its transcription, whereas Twist repress E-cadherin indirectly [23]. In present study, we examined chemoresistance was associated with the enhanced EMT in H69AR cells.…”

Section: Discussionmentioning

confidence: 99%

Emodin: One Main Ingredient of Shufeng Jiedu Capsule Reverses Chemoresistance of Lung Cancer Cells Through Inhibition of EMT

Yuan

Liao²,

Xue

et al. 2017

Cell Physiol Biochem

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Background: Chemoresistance has become a an important worldwide problem to cancer treatment. Understanding the mechanism of drug resistance is the key to solve this problem and improve the survival of the patient. Doxorubicin and its analogues are widely used as antitumor drugs but many doxorubicin resistant cases have been identified in recent years. Doxorubicin (Dox) resistance is a very serious phenomenon in lung cancer treatment. As we could show previously, Shufeng Jiedu Capsule (SFJDC) can effectively reverse H69AR cells resistance to Dox, thus, the present study was designed to explore the mechanism underlying the effects of the main ingredient Emodin on chemosensitivity of H69AR cells to Dox. Methods: First, the growth inhibition rate of lung cancer cells and normal bronchial epithelial cells (BECs) was determined by MTT. Then, the resistance-induced epithelial-mesenchymal transition (EMT) of H69AR cells was examined by western blot and the effect of Emodin on Twist, Snail or Slug was assayed by Real-time PCR and Western blot. The activation of NF-kappa B was assayed by Western blot. Proliferation, apoptosis, migration and invasion of H69AR cells induced by Twist, Snail and Slug were also assayed by flow cytometry and transwell chamber. Results: The results showed that after administration of Dox (10µM) with different concentrations of Emodin, the cells exhibited a dose-dependent inhibition action to H69AR cells at 48 hours. H69AR induced the expression of Twist, Snail, and Slug when compared with Dox-sensitive H69 cells. The expression of Twist, Snail, and Slug can be effectively inhibited by combination of Dox and Emodin. The reversal of resistance was associated with the inhibition of NF-kappa B. Twist, Snail and Slug promoted proliferation, migration and invasion and inhibited apoptosis. Conclusion: Our data suggest that Emodin can effectively reverse the resistance of H69AR to Dox, an effect paralleled by inhibition of EMT, cell proliferation, apoptosis, migration and invasion.

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“…Traditional tumor therapy mainly includes physical therapy for the macroscopic tumor body and chemotherapy for microcosmic tumor cells . These methods always suffer from the low efficiency, high systemic toxicity, and severe effects on quality of life . Recently, the biological application of nanomaterials has received much attention .…”

Section: Introductionmentioning

confidence: 99%

Emancipating Target‐Functionalized Carbon Dots from Autophagy Vesicles for a Novel Visualized Tumor Therapy

Yang

Deng

et al. 2018

Adv Funct Materials

113

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Killing the tumor cells by a visualized targeting system is a promising strategy with which to achieve high efficiency, low side effects, and a high survival rate for tumor therapy. Here, an autophagy regulation strategy is reported by emancipating target-functionalized carbon dots from autophagy vesicles for the efficient visualized tumor therapy. The folic acid modified N-doped carbon dots (FN-CDs) are selectively endocytosed (specific cellular uptake rate >93.40%) and stably existed in autophagic vacuoles in tumor cells. Next, the autophagic vacuoles are "opened" by the autophagy inhibitors. Released FN-CDs activate both the intrinsic and extrinsic apoptotic signaling pathway and kill tumor cells efficiently. This method achieves therapeutic effects with high performance in 26 types of tumor cell lines. Animal experiments show that the 30 d survival rate of this therapeutic strategy is much higher than that with traditional drug treatment. Real-time imaging/monitoring and its effects on the intelligent tumor therapy are also demonstrated based on the stable, strong, green emission from FN-CDs.

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TRPP2 Enhances Metastasis by Regulating Epithelial-Mesenchymal Transition in Laryngeal Squamous Cell Carcinoma

Cited by 36 publications

References 38 publications

Stabilization of Slug by NF-κB is Essential for TNF-α -Induced Migration and Epithelial-Mesenchymal Transition in Head and Neck Squamous Cell Carcinoma Cells

Stabilization of Slug by NF-κB is Essential for TNF-α -Induced Migration and Epithelial-Mesenchymal Transition in Head and Neck Squamous Cell Carcinoma Cells

Emodin: One Main Ingredient of Shufeng Jiedu Capsule Reverses Chemoresistance of Lung Cancer Cells Through Inhibition of EMT

Emancipating Target‐Functionalized Carbon Dots from Autophagy Vesicles for a Novel Visualized Tumor Therapy

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