RETRACTED: Schizandrin A enhances chemosensitivity of colon carcinoma cells to 5-fluorouracil through up-regulation of miR-195

Kong, Dongfang; Zhang, Deyong; Chu, Xianqun; Wang, Jing

doi:10.1016/j.biopha.2018.01.035

Cited by 33 publications

(23 citation statements)

References 29 publications

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“…Its high expression level indicates poor overall survival and free of progression [66] Cisplatin/gemcitabine Modulating miR-196a-5p of bladder carcinoma cells NCRAN [67] Cisplatin Upregulating drug resistance; suppressing apoptosis LET/NF90/miR-145 [68] Gemcitabine Upregulating TGFβ1 GAS5 [69] Doxorubicin Promoting apoptosis; depressing the expression of anti-apoptosis protein Bcl-2 Lung cancer HOTAIR Crizotinib [70] Activating autophagy by inhibiting the phosphorylation of ULK1 Gefitinib [71] Activating Bax/Caspase-3 and TGF-α/EGFR signaling AK126698 [72] Cisplatin Suppressing canonical Wnt signaling pathway; downregulating cisplatin resistance MEG3 [41] Cisplatin Enhancing cisplatin sensitivity via regulating miR-21-5p/SOX7 axis; activating p53 and Bcl-xl of LAD cells XIST [32] Cisplatin Enhancing the drug resistance of NSCLC cells via suppressing autophagy AK001796 [73] Cisplatin Upregulating the expression of ANRIL KCNQ1OT1 [74] Paclitaxel Upregulating the chemoresistance MIAT [9] Gefitinib Regulating miR-34a TUG1 [75] Cisplatin Regulating LIMK2b via EZH2 ANRIL [76] Cisplatin Inhibits proliferation, induces apoptosis Colorectal cancer H19 [77] Doxorubicin Overexpression of H19 activating Wnt/β-catenin pathway CUDR [78] 5-fluorouracil Upregulating miR-195 Oxaliplatin…”

Section: Mutations Of Drug Targetsmentioning

confidence: 99%

Recent Progress in Characterizing Long Noncoding RNAs in Cancer Drug Resistance

Zhao¹,

Shan²,

He³

et al. 2019

J. Cancer

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Drug resistance is an important cause of failure in cancer chemotherapies. A large number of long noncoding RNAs (lncRNAs) have been found to be related to drug resistance in cancers. Therefore, lncRNAs provide potential targets for cancer therapies. The lncRNAs involved in cancer drug resistance are attracting interest from an increasing number of researchers. This review summarizes the latest research on the mechanisms and functions of lncRNAs in cancer drug resistance and envisages their future developments and therapeutic applications. This research suggests that lncRNAs regulate drug resistance through multiple mechanisms. LncRNAs do not affect drug resistance directly; usually, they do so by regulating the expression of some intermediate regulatory factors. In addition, lncRNAs exhibit a diversity of functions in cancer drug resistance. The overexpression of most lncRNAs promotes drug resistance, while a few lncRNAs have inhibitory effects.

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Section: Mutations Of Drug Targetsmentioning

confidence: 99%

Recent Progress in Characterizing Long Noncoding RNAs in Cancer Drug Resistance

Zhao¹,

Shan²,

He³

et al. 2019

J. Cancer

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“…The antitumor effects of Sch A were well-studied in several recent investigations. As a major member of dibenzocyclooctadiene lignans, Sch A not only impaired the proliferation, migration, and invasion of breast cancer, ovarian cancer, and thyroid cancer through prompting ER stress, inactivating Akt signals, and down-regulating miR-429, but also acted as a favorable chemosensitization agent in breast cancer and colon carcinoma [18,19,39,40]. Moreover, Xian et al [41] surprisingly found that Sch A could even improve the gefitinib resistance in non-small cell lung cancer cells (NSCLC) via inhibition of IKKβ/NF-κB signaling.…”

Section: Discussionmentioning

confidence: 99%

Schizandrin A exhibits potent anticancer activity in colorectal cancer cells by inhibiting heat shock factor 1

Chen

Zheng

et al. 2020

Bioscience Reports

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Heat shock factor 1 (HSF1) is a powerful multifaceted oncogenic modifier that plays a role in maintaining the protein balance of cancer cells under various stresses. In recent studies, there have been reports of increased expression of HSF1 in colorectal cancer (CRC) cells, and the depletion of the HSF1 gene knockdown has inhibited colon cancer growth both in vivo and in vitro. Therefore, HSF1 is a promising target for colon cancer treatment and chemoprevention. In the present study, we found that Schizandrin A (Sch A) significantly inhibited the growth of CRC cell lines by inducing cell cycle arrest, apoptosis and death. Through HSE luciferase reporter assay and quantitative PCR (qPCR), we identified Sch A as a novel HSF1 inhibitor. In addition, Sch A could effectively inhibit the induction of HSF1 target proteins such as heat-shock protein (HSP) 70 (HSP70) and HSP27, whether in heat shock or normal temperature culture. In the Surface Plasmon Resonance (SPR) experiment, Sch A showed moderate affinity with HSF1, further confirming that Sch A might be a direct HSF1 inhibitor. The molecular docking and molecular dynamic simulation results of HSF1/Sch A suggested that Sch A formed key hydrogen bond and hydrophobic interactions with HSF1, which may contribute to its potent HSF1 inhibition. These findings provide clues for the design of novel HSF1 inhibitors and drug candidates for colon cancer treatment.

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“…Other lignans, such as schizandrin A, isolated from Schisandra chinensis fruits enhanced chemosensitivity of colorectal carcinoma cells to 5-FU through upregulation of miR-195. In addition, upregulation of miR-195 inactivated NF-κB and PI3K/AKT signaling pathways [48]. Silybin is the major active constituent of silymarin (a mixture of flavonolignans) from milk thistle fruits.…”

Section: Lignansmentioning

confidence: 99%

Alleviation of Multidrug Resistance by Flavonoid and Non-Flavonoid Compounds in Breast, Lung, Colorectal and Prostate Cancer

Costea

Vlad

Miclea

et al. 2020

IJMS

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The aim of the manuscript is to discuss the influence of plant polyphenols in overcoming multidrug resistance in four types of solid cancers (breast, colorectal, lung and prostate cancer). Effective treatment requires the use of multiple toxic chemotherapeutic drugs with different properties and targets. However, a major cause of cancer treatment failure and metastasis is the development of multidrug resistance. Potential mechanisms of multidrug resistance include increase of drug efflux, drug inactivation, detoxification mechanisms, modification of drug target, inhibition of cell death, involvement of cancer stem cells, dysregulation of miRNAs activity, epigenetic variations, imbalance of DNA damage/repair processes, tumor heterogeneity, tumor microenvironment, epithelial to mesenchymal transition and modulation of reactive oxygen species. Taking into consideration that synthetic multidrug resistance agents have failed to demonstrate significant survival benefits in patients with different types of cancer, recent research have focused on beneficial effects of natural compounds. Several phenolic compounds (flavones, phenolcarboxylic acids, ellagitannins, stilbens, lignans, curcumin, etc.) act as chemopreventive agents due to their antioxidant capacity, inhibition of proliferation, survival, angiogenesis, and metastasis, modulation of immune and inflammatory responses or inactivation of pro-carcinogens. Moreover, preclinical and clinical studies revealed that these compounds prevent multidrug resistance in cancer by modulating different pathways. Additional research is needed regarding the role of phenolic compounds in the prevention of multidrug resistance in different types of cancer.

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RETRACTED: Schizandrin A enhances chemosensitivity of colon carcinoma cells to 5-fluorouracil through up-regulation of miR-195

Cited by 33 publications

References 29 publications

Recent Progress in Characterizing Long Noncoding RNAs in Cancer Drug Resistance

Recent Progress in Characterizing Long Noncoding RNAs in Cancer Drug Resistance

Schizandrin A exhibits potent anticancer activity in colorectal cancer cells by inhibiting heat shock factor 1

Alleviation of Multidrug Resistance by Flavonoid and Non-Flavonoid Compounds in Breast, Lung, Colorectal and Prostate Cancer

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