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Astragaloside IV Induced miR-134 Expression Reduces EMT and Increases Chemotherapeutic Sensitivity by Suppressing CREB1 Signaling in Colorectal Cancer Cell Line SW-480.

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BACKGROUND Colorectal cancer (CRC) is one of the leading causes of cancer-related deaths worldwide. Although chemotherapy is the primary means in colorectal cancer treatment, it is burdenerd by adverse drug effects. Drug-resistance is one of the most important challenges for chemotherapy and

Astragaloside IV downregulates the expression of MDR1 in Bel‑7402/FU human hepatic cancer cells by inhibiting the JNK/c‑Jun/AP‑1 signaling pathway.

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Previous studies demonstrated that astragaloside IV (ASIV) is a potential P‑glycoprotein (P‑gp)‑mediated multidrug resistance (MDR) reversal agent through mechanisms involving downregulation of the gene expression of mdr1. In order to investigate whether the c‑Jun N‑terminal kinase (JNK) signaling

Astragaloside IV inhibits the invasion and metastasis of SiHa cervical cancer cells via the TGF‑β1‑mediated PI3K and MAPK pathways.

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Astragaloside IV is the main ingredient of the medicinal herb Radix astragali, which has reported to have antitumor activity in vitro and in vivo. To determine whether the inhibitory effect of astragaloside IV on the invasion and metastasis of the cervical cancer cells is associated with

Astragaloside IV increases MMP-2 mRNA and protein expression in human lung cancer A549 cells.

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Lung cancer is the leading cause of cancer-related death in Taiwan. In the clinical treatment of lung cancer patients in Asia, an Astragalus-based herbal mixture is commonly used in conjunction with chemotherapy. The principal component of Astragalus (also known as Huang-qi) is Astragaloside IV. The

Astragaloside IV enhances taxol chemosensitivity of breast cancer via caveolin-1-targeting oxidant damage.

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Accumulating evidence suggests that caveolin-1 (CAV-1) is a stress-related oncotarget and closely correlated to chemoresistance. Targeting CAV-1 might be a promising strategy to improve chemosensitivity for breast cancer treatment. Astragaloside IV (AS-IV), a bioactive compound purified from

Astragaloside IV Enhances Cisplatin Chemosensitivity in Non-Small Cell Lung Cancer Cells Through Inhibition of B7-H3.

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BACKGROUND Chemoresistance is a major obstacle to successful chemotherapy for human non-small cell lung cancer (NSCLC). Astragaloside IV, the component of Astragalus membranaceus, has been reported to exhibit anti-inflammation, anti-cancer and immunoregulatory properties. In the present study, we

Astragaloside IV inhibits progression of lung cancer by mediating immune function of Tregs and CTLs by interfering with IDO.

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OBJECTIVE Tumor cells have developed multiple mechanisms to escape immune recognition mediated by T cells. Indoleamine 2,3-dioxygenase (IDO), a tryptophan-catabolizing enzyme inducing immune tolerance, is involved in tumor escape from host immune systems in mice. Astragaloside IV (AS-IV), an extract

Astragaloside IV inhibits breast cancer cell invasion by suppressing Vav3 mediated Rac1/MAPK signaling.

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BACKGROUND Astragaloside IV (AS-IV), the major active triterpenoid in Radix Astragali, has shown anti-tumorigenic properties in certain cancers; however, its role in breast cancer remains unclear. The present study investigated the effects of AS-IV on breast cancer in vitro and in vivo and examined

Astragaloside IV inhibits pathological functions of gastric cancer-associated fibroblasts.

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OBJECTIVE To investigate the inhibitory effect of astragaloside IV on the pathological functions of cancer-associated fibroblasts, and to explore the underlying mechanism. METHODS Paired gastric normal fibroblast (GNF) and gastric cancer-associated fibroblast (GCAF) cultures were established from

Astragaloside IV inhibits the progression of non-small cell lung cancer through Akt/GSK-3β/β-catenin pathway.

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Astragaloside IV (AS-IV) is an active ingredient in Astragalus membranaceus, and involved in various biological processes, such as regulating the immune system, and counteracting inflammation and malignancy. The aim of this study was to explore the effect of AS-IV on non-small cell lung cancer

Astragaloside IV inhibits cell proliferation of colorectal cancer cell lines through down-regulation of B7-H3.

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Astragaloside IV showed a pivotal anti-cancer efficacy in multiple types of cancers and reversed chemoresistance in colorectal cancer (CRC). However, it remained unknown whether and how Astragaloside IV suppressed the progression of CRC. In the present study, we found that Astragaloside IV treatment

Astragaloside IV sensitizes non-small cell lung cancer cells to gefitinib potentially via regulation of SIRT6.

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Astragaloside IV, the active component of Astragalus membranaceus, exhibits diverse biological roles including the anti-tumor activity. In this study, we evaluated the chemosensitive role of astragaloside IV in non-small cell lung cancer cells. Cell Counting Kit-8 analysis was performed to determine

Astragaloside IV sensitizes non-small cell lung cancer cells to cisplatin by suppressing endoplasmic reticulum stress and autophagy

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Background: Cisplatin is an effective chemotherapeutic drug for treating various cancers including non-small cell lung cancer (NSCLC), but resistance to cisplatin remains the main limitation to its use in clinic. Astragaloside IV (AS-IV),

Quantitative proteomics analysis of differentially expressed proteins induced by astragaloside IV in cervical cancer cell invasion.

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Background

Cervical cancer remains the second leading cause of mortality in women in developing countries. While surgery, chemotherapy, radiotherapy, and vaccine therapy are being applied for its treatment, individually or in combination, the survival rate in advanced cervical

Astragaloside IV Enhances Cisplatin Chemosensitivity in Human Colorectal Cancer via Regulating NOTCH3.

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Although astragaloside IV exhibits anti-inflammation, immunoregulatory, and anticancer properties, the chemosensitization effects of astragaloside IV in colorectal cancer have never been reported. Our study tested whether astragaloside could increase cisplatin sensitivity in colorectal cancer. CCK-8

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