scholarly journals Astragaloside IV Downregulates β-Catenin in Rat Keratinocytes to Counter LiCl-Induced Inhibition of Proliferation and Migration

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Fu-Lun Li ◽  
Xin Li ◽  
Yi-Fei Wang ◽  
Xiu-Li Xiao ◽  
Rong Xu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Molecular Mechanisms ◽  
Colorimetric Assay ◽  
Wnt Signaling Pathway ◽  
Nuclear Antigen ◽  
Astragaloside Iv ◽  
Inhibition Of Proliferation ◽  
And Migration ◽  
Proliferation And Migration

Re-epithelialization is a crucial step towards wound healing. The traditional Chinese medicine,Astragalus membranaceus(Fisch) Bge, has been used for hundreds of years for many kinds of ulcerated wounds. Recent research has identified the active compound in this drug as astragaloside IV (AS-IV), but the underlying molecular mechanisms of its therapeutic action on keratinocytes remain poorly understood. In this study, we used anin vitromodel of ulcer-like wound processes, lithium chloride (LiCl)-induced cultured mouse keratinocytes, to investigate the effects of AS-IV treatment. The effects on cell proliferation were evaluated by the MTS/PMS colorimetric assay, effects on cell migration were determined by a wound-healing scratch experiment, effects on the cell cycle were analyzed by flow cytometry, and effects on protein expression were analyzed by immunoblotting and immunofluorescence. LiCl strongly inhibited cell proliferation and migration, up-regulatedβ-catenin expression, and down-regulated proliferating cell nuclear antigen (PCNA) expression. AS-IV treatment attenuat the inhibition of proliferation and migration, significantly reducing the enhancedβ-catenin expression, and recovering PCNA andβ-tubulin expression. Thus, AS-IV mediates mouse keratinocyte proliferation and migrationviaregulation of the Wnt signaling pathway. Down-regulatingβ-catenin to increase keratinocyte migration and proliferation is one mechanism by which AS-IV can promote ulcerated wound healing.

scholarly journals TIPE Regulates DcR3 Expression and Function by Activating the PI3K/AKT Signaling Pathway in CRC

2021 ◽  
Vol 10 ◽  
Author(s):  
Mengya Zhong ◽  
Xingfeng Qiu ◽  
Yu Liu ◽  
Yan Yang ◽  
Lei Gu ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Akt Signaling ◽  
Luciferase Reporter ◽  
Akt Signaling Pathway ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Hct116 Cells ◽  
Proliferation And Migration

Tumor necrosis factor-induced protein-8 (TIPE) is highly expressed in colorectal cancer (CRC). Decoy receptor 3 (DcR3) is a soluble secreted protein that can antagonize Fas ligand (FasL)-induced apoptosis and promote tumorigenesis. It remains unclear whether TIPE can regulate DcR3 expression. In this study, we examined this question by analyzing the relationship between these factors in CRC. Bioinformatics and tissue microarrays were used to determine the expression of TIPE and DcR3 and their correlation in CRC. The expression of TIPE and DcR3 in colon cancer cells was detected. Plasma samples were collected from CRC patients, and DcR3 secretion was measured. Then, dual-luciferase reporter gene analysis was performed to assess the interaction between TIPE and DcR3. We exogenously altered TIPE expression and analyzed its function and influence on DcR3 secretion. Lipopolysaccharide (LPS) was used to stimulate TIPE-overexpressing HCT116 cells, and alterations in signaling pathways were detected. Additionally, inhibitors were used to confirm molecular mechanisms. We found that TIPE and DcR3 were highly expressed in CRC patients and that their expression levels were positively correlated. DcR3 was highly expressed in the plasma of cancer patients. We confirmed that TIPE and DcR3 were highly expressed in HCT116 cells. TIPE overexpression enhanced the transcriptional activity of the DcR3 promoter. TIPE activated the PI3K/AKT signaling pathway to regulate the expression of DcR3, thereby promoting cell proliferation and migration and inhibiting apoptosis. In summary, TIPE and DcR3 are highly expressed in CRC, and both proteins are associated with poor prognosis. TIPE regulates DcR3 expression by activating the PI3K/AKT signaling pathway in CRC, thus promoting cell proliferation and migration and inhibiting apoptosis. These findings may have clinical significance and promise for applications in the treatment or prognostication of CRC.

scholarly journals In Vitro Wound Healing Potential of Flavonoid C-Glycosides from Oil Palm (Elaeis guineensis Jacq.) Leaves on 3T3 Fibroblast Cells

Antioxidants ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 326 ◽  
Author(s):  
Mohamad Shazeli Che Zain ◽  
Soo Yee Lee ◽  
Murni Nazira Sarian ◽  
Sharida Fakurazi ◽  
Khozirah Shaari
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Oil Palm ◽  
Elaeis Guineensis ◽  
Fibroblast Cells ◽  
Crude Extracts ◽  
Elaeis Guineensis Jacq ◽  
And Migration ◽  
Proliferation And Migration

Oil palm (Elaeis guineensis Jacq.) leaves (OPL) are widely available at zero cost in Southeast Asia countries, especially in Malaysia and Indonesia due to large scale oil palm plantations. OPLs contain a large amount of flavonoids in particular flavonoid C-glycosides, which are known to possess useful biological properties including antioxidant and wound healing properties. The present study aimed at evaluating the wound healing efficacy of OPL in various solvent extracts and flavonoid enriched fractions and to determine the contribution of flavonoid C-glycosides (orientin, isoorientin, vitexin and isovitexin) using in-vitro scratch assay on 3T3 fibroblast cells. Solvent crude extracts with different polarity were screened and the most active extract was subjected to acid hydrolysis. The crude and acid hydrolysed extracts were further enriched using macroporous resins, XAD7HP. UHPLC-UV/PDA and LC-MS/MS analysis were applied for identification and confirmation of flavonoid C-glycosides. The wound healing properties comprised of cell viability, cell proliferation and cell migration were studied. Allantoin was used as a positive control to compare the efficacy among the tested samples. The results revealed all OPL crude extracts, flavonoid enriched fractions and flavonoid C-glycosides were non-toxic at concentrations below 25 µg/mL and showed better cell proliferation and migration activities at low concentrations than higher concentrations.. This study also demonstrated orientin, isoorientin, vitexin and isovitexin presented in OPL extracts and flavonoid enriched fractions stimulated proliferation and migration of 3T3 fibroblast cells. Hence, these findings may pose potential therapeutic bioactive agents for wound healing by enhancing fibroblast proliferation and migration.

scholarly journals LncRNA XIST promotes extracellular matrix synthesis, proliferation and migration by targeting miR-29b-3p/COL1A1 in human skin fibroblasts after thermal injury

2019 ◽  
Vol 52 (1) ◽  
Author(s):  
Wei Cao ◽  
Youping Feng
Keyword(s):  
Extracellular Matrix ◽  
Cell Proliferation ◽  
Wound Healing ◽  
Western Blot ◽  
Thermal Injury ◽  
Human Skin Fibroblasts ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Long noncoding RNAs (lncRNAs) have been reported to be associated with dermis process during burn wound healing. This study aimed to investigate the role of lncRNA X-inactive specific transcript (XIST) in human skin fibroblasts (HSF) and extracellular matrix (ECM) as well as the regulatory network of XIST/microRNA-29b-3p (miR-29b-3p)/collagen 1 alpha 1 (COL1A1). Methods The wound samples were collected from 25 patients with deep partial thickness burn at day 5 after burn. The thermal injured model was established using HSF cells. The expressions of XIST, miR-29b-3p and COL1A1 were measured by quantitative real-time polymerase chain reaction and western blot. ECM synthesis, cell proliferation and migration were detected by western blot, cell counting kit-8 and trans-well assays, respectively. The interaction between miR-29b-3p and XIST or COL1A1 was explored by bioinformatics analysis and luciferase reporter assay. Results The expressions of XIST and COL1A1 were enhanced but miR-29b-3p expression was decreased after thermal injury. XIST overexpression promoted ECM synthesis, cell proliferation and migration in thermal injured HSF cells. However, XIST knockdown played an opposite effect. miR-29b-3p overexpression inhibited ECM synthesis, cell proliferation and migration, which was reversed by XIST. COL1A1 silence suppressed ECM synthesis, cell proliferation and migration by miR-29b-3p targeting. Moreover, COL1A1 up-regulation weakened the effect of XIST silence on ECM synthesis and HSF cell function. Conclusion XIST promoted ECM synthesis, cell proliferation and migration by sponging miR-29b-3p and targeting COL1A1 in HSF cells after thermal injury, indicating the promoting role of XIST in wound healing.

scholarly journals Inhibition of Carnitine Palmitoyl Transferase 1A-induced Fatty Acid Oxidation Suppresses Cell Progression in Gastric Cancer

2020 ◽  
Author(s):  
Liqiang Wang ◽  
Changfeng Li ◽  
Yumei Song ◽  
ZhenKun Yan
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Progression ◽  
Molecular Mechanisms ◽  
High Rate ◽  
Acid Oxidation ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background: Gastric cancer (GC) has a high rate of metastasis which thereason leading to death. Carnitine palmitoyltransferase 1a (CPT1A) has been reported to play a critical obstacle to various types of cancer progression, which is an attractive focus in anti-cancer therapy. However, the underlying molecular mechanisms of CPT1A involved in GC have not been clarified unclear.Methods: To determine the expression of CPT1A in human GC tissues and cells and illustrate whether it is correlated with the clinical pathologic characteristics and prognosis in GC patients. Its roles and potential mechanisms in regulating tumor growth and invasion were evaluated by CPT1A knockdown/overexpression of GC cells in vitro.Results: Marked upregulation of CPT1A protein expression was observed in GC cells and tissues, which was associated with grade, pathological stage, lymph node metastasis and poor prognosis in patients with GC. CPT1A overexpression also promoted the proliferation, invasion, EMT process of GC cells. In addition, CPT1A upregulation activated GC cell FAO via increasing NADP+/NADPH ratio, whereasinhibiting of FAO abolished the effects of CPT1A on GC cell proliferation and migration.Conclusion: Our results examine that CPT1A-mediated FAO activation increases GC cell proliferation and migration, supporting that CPT1A is a useful prognostic biomarker and an attractive focus for GC.

scholarly journals Inhibition of carnitine palmitoyl transferase 1A-induced fatty acid oxidation suppresses cell progression in gastric cancer

2020 ◽  
Author(s):  
Liqiang Wang ◽  
Changfeng Li ◽  
Yumei Song ◽  
ZhenKun Yan
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Molecular Mechanisms ◽  
High Rate ◽  
Acid Oxidation ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background: Gastric cancer (GC) has a high rate of metastasis which thereason leading to death. Carnitine palmitoyltransferase 1a (CPT1A) has been reported to play a critical obstacle to various types of cancer progression, which is an attractive focus in anti-cancer therapy. However, the underlying molecular mechanisms of CPT1A involved in GC have not been clarified unclear. Methods: To determine the expression of CPT1A in human GC tissues and cells and illustrate whether it is correlated with the clinical pathologic characteristics and prognosis in GC patients. Its roles and potential mechanisms in regulating tumor growth and invasion were evaluated by CPT1A knockdown/overexpression of GC cells in vitro . Results: Marked upregulation of CPT1A protein expression was observed in GC cells and tissues, which was associated with grade, pathological stage, lymph node metastasis and poor prognosis in patients with GC. CPT1A overexpression also promoted the proliferation, invasion, EMT process of GC cells. In addition, CPT1A upregulation activated GC cell FAO via increasing NADP + /NADPH ratio, whereas inhibiting of FAO abolished the effects of CPT1A on GC cell proliferation and migration. Conclusion: Our results examine that CPT1A-mediated FAO activation increases GC cell proliferation and migration, supporting that CPT1A is a useful prognostic biomarker and an attractive focus for GC. Keywords: CPT1A; gastric cancer; fatty acid oxidation; prognostic; progression

scholarly journals c-Jun Overexpression Accelerates Wound Healing in Diabetic Rats by Human Umbilical Cord-Derived Mesenchymal Stem Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Chun Yue ◽  
Zi Guo ◽  
Yufang Luo ◽  
Jingjing Yuan ◽  
Xinxing Wan ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Growth Factor ◽  
Wound Closure ◽  
Human Umbilical Cord ◽  
Diabetic Wound ◽  
Diabetic Wound Healing ◽  
And Migration ◽  
Proliferation And Migration

Objective. Mesenchymal stem cells (MSCs) are considered a promising therapy for wound healing. Here, we explored the role of c-Jun in diabetic wound healing using human umbilical cord-derived MSCs (hUC-MSCs). Methods. Freshly isolated hUC-MSCs were subjected to extensive in vitro subcultivation. The cell proliferative and migratory capacities were assessed by the Cell Counting Kit-8 and scratch assays, respectively. c-Jun expression was evaluated by RT-PCR and western blot analysis. The function of c-Jun was investigated with lentivirus transduction-based gene silencing and overexpression. Diabetes mellitus was induced in SD rats on a high-glucose/fat diet by streptozocin administration. Wounds were created on the dorsal skin. The effects of c-Jun silencing and overexpression on wound closure by hUC-MSCs were examined. Reepithelialization and angiogenesis were assessed by histological and immunohistochemical analysis, respectively. Platelet-derived growth factor A (PDGFA), hepatocyte growth factor (HGF), and vascular endothelial growth factor (VEGF) levels were determined by western blot analysis. Results. hUC-MSCs showed gradually decreased cell proliferation, migration, and c-Jun expression during subcultivation. c-Jun silencing inhibited cell proliferation and migration, while c-Jun overexpression enhanced proliferation but not migration. Compared with untransduced hUC-MSCs, local subcutaneous injection of c-Jun-overexpressing hUC-MSCs accelerated wound closure, enhanced angiogenesis and reepithelialization at the wound bed, and increased PDGFA and HGF levels in wound tissues. Conclusion. c-Jun overexpression promoted hUC-MSC proliferation and migration in vitro and accelerated diabetic wound closure, reepithelization, and angiogenesis by hUC-MSCs in vivo. These beneficial effects of c-Jun overexpression in diabetic wound healing by hUC-MSCs were at least partially mediated by increased PDGFA and HGF levels in wound tissues.

scholarly journals Wound healing promoting activity of Earthworm, Eutyphoeus gammiei (Beddard): in vitro studies on human skin keratinocyte cell line (HaCat).

2018 ◽  
Vol 8 (6) ◽  
pp. 155-158
Author(s):  
Susmita Saha ◽  
Deepjyoti Bhattacharjee ◽  
Anwesha Saha ◽  
Gahin De ◽  
Partha Saha ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Wound Healing ◽  
Cell Line ◽  
Key Factors ◽  
Cell Proliferation And Migration ◽  
Keratinocyte Cell Line Hacat ◽  
Keratinocyte Cell ◽  
And Migration ◽  
Proliferation And Migration

Earthworm, Eutyphoeus gammiei, homogenate (EGH) was screened for wound healing activity on human keratinocyte cell line, HaCat, by cell proliferation and migration assays. The maximum proliferation and migration of keratinocyte cells were observed at the dose of 25μg/ml. As cell proliferation and migration are key factors for wound healing, the study clearly suggests the potential role of earthworm species Eutyphoeus gammiei on wound healing. Keywords: Eutyphoeus gammiei, Keratinocyte, MTT assay, scratch assay.

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