&lt;p&gt;Curcumin Affects Gastric Cancer Cell Migration, Invasion and Cytoskeletal Remodeling Through Gli1-β-Catenin&lt;/p&gt;

Zhang, Xiao; Zhang, Chen-Li; Ren, Zhiheng; Zhang, Fangfang; Xu, Jianrong; Zheng, Haixue

doi:10.2147/cmar.s244384

Cited by 33 publications

(19 citation statements)

References 59 publications

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“…Affymetrix microarray results suggest that cytoskeletal remodeling and the Wnt signaling pathway are the two of the top pathways disrupted by ERp57 silencing in HeLa cells [99]. The present data demonstrate that β-catenin participates in the mechanisms of cell adhesion, cytoskeleton remodeling and the canonical Wnt signaling pathway [100]. Stable knockdown of ERp57 induces β-catenin accumulation and inhibits the migration of HeLa cells [99], and resveratrol can increase the interaction between ERp57 and β-catenin [101].…”

Section: Regulation Of Other Signal Transduction Pathwaysmentioning

confidence: 52%

Insights into the role of ERp57 in cancer

Song¹,

Líu²,

Wu³

et al. 2021

J. Cancer

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Endoplasmic reticulum resident protein 57 (ERp57) has a molecular weight of 57 kDa, belongs to the protein disulfide-isomerase (PDI) family, and is primarily located in the endoplasmic reticulum (ER). ERp57 functions in the quality control of nascent synthesized glycoproteins, participates in major histocompatibility complex (MHC) class I molecule assembly, regulates immune responses, maintains immunogenic cell death (ICD), regulates the unfolded protein response (UPR), functions as a 1,25-dihydroxy vitamin D3 (1,25(OH)2D3) receptor, regulates the NF-κB and STAT3 pathways, and participates in DNA repair processes and cytoskeletal remodeling. Recent studies have reported ERp57 overexpression in various human cancers, and altered expression and aberrant functionality of ERp57 are associated with cancer growth and progression and changes in the chemosensitivity of cancers. ERp57 may become a potential biomarker and therapeutic target to combat cancer development and chemoresistance. Here, we summarize the available knowledge of the role of ERp57 in cancer and the underlying mechanisms.

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Section: Regulation Of Other Signal Transduction Pathwaysmentioning

confidence: 52%

Insights into the role of ERp57 in cancer

Song¹,

Líu²,

Wu³

et al. 2021

J. Cancer

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“…Curcumin can impair both proliferation and metastasis of cancer cells via inducing cell cycle arrest, triggering cytoskeletal remodeling and inhibiting epithelial-to-mesenchymal transition (EMT). In this way, molecular pathways such as Wnt and Shh that are involved in cancer progression, undergo downregulation upon curcumin administration [ 46 ]. The inhibitory effect of curcumin on viability and colony formation of cancer cells is vital for enhancing sensitivity of cancer cells into chemotherapy [ 47 ].…”

Section: Antitumor Activity Of Curcumin: In Vitro In Vivo and CLImentioning

confidence: 99%

Polychemotherapy with Curcumin and Doxorubicin via Biological Nanoplatforms: Enhancing Antitumor Activity

et al. 2020

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Doxorubicin (DOX) is a well-known chemotherapeutic agent extensively applied in the field of cancer therapy. However, similar to other chemotherapeutic agents such as cisplatin, paclitaxel, docetaxel, etoposide and oxaliplatin, cancer cells are able to obtain chemoresistance that limits DOX efficacy. In respect to dose-dependent side effect of DOX, enhancing its dosage is not recommended for effective cancer chemotherapy. Therefore, different strategies have been considered for reversing DOX resistance and diminishing its side effects. Phytochemical are potential candidates in this case due to their great pharmacological activities. Curcumin is a potential antitumor phytochemical isolated from Curcuma longa with capacity of suppressing cancer metastasis and proliferation and affecting molecular pathways. Experiments have demonstrated the potential of curcumin for inhibiting chemoresistance by downregulating oncogene pathways such as MMP-2, TGF-β, EMT, PI3K/Akt, NF-κB and AP-1. Furthermore, coadministration of curcumin and DOX potentiates apoptosis induction in cancer cells. In light of this, nanoplatforms have been employed for codelivery of curcumin and DOX. This results in promoting the bioavailability and internalization of the aforementioned active compounds in cancer cells and, consequently, enhancing their antitumor activity. Noteworthy, curcumin has been applied for reducing adverse effects of DOX on normal cells and tissues via reducing inflammation, oxidative stress and apoptosis. The current review highlights the anticancer mechanism, side effects and codelivery of curcumin and DOX via nanovehicles.

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“…In addition to MMP downregulation, curcumin also exerts an influence on epithelial-mesenchymal transition (EMT), which is a pivotal event that generates prometastatic cell types in cancers. 47 , 48 It was demonstrated that curcumin inhibits HGF-induced EMT in lung cancer via modulation of c-Met, which functions upstream of PI3K/Akt/mTOR signaling. 49 The potential regulatory axis was further verified in HUVECs treated with curcumin, which had impaired tubular formation ability in vitro.…”

Section: Mechanisms Of Curcumin-mediated Lung Cancer Suppressionmentioning

confidence: 99%

Nanoscale Formulations: Incorporating Curcumin into Combination Strategies for the Treatment of Lung Cancer

Wu¹,

Ou²,

Shang³

et al. 2021

DDDT

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Lung cancer remains the most common cancer worldwide. Although significant advances in screening have been made and early diagnosis strategies and therapeutic regimens have been developed, the overall survival rate remains bleak. Curcumin is extracted from the rhizomes of turmeric and exhibits a wide range of biological activities. In lung cancer, evidence has shown that curcumin can markedly inhibit tumor growth, invasion and metastasis, overcome resistance to therapy, and even eliminate cancer stem cells (CSCs). Herein, the underlying molecular mechanisms of curcumin were summarized by distinct biological processes. To solve the limiting factors that curtail the clinical applications of curcumin, nanoformulations encapsulating curcumin were surveyed in detail. Nanoparticles, including liposomes, micelles, carbon nanotubes (CNTs), solid lipid nanoparticles (SLNs), nanosuspensions, and nanoemulsions, were explored as proper carriers of curcumin. Moreover, it was firmly verified that curcumin has the ability to sensitize lung cancer cells to chemotherapeutic drugs, such as cisplatin and docetaxel, and to various targeted therapies. Regarding the advantages and drawbacks of curcumin, we concluded that combination therapy based on nanoparticles would be the optimal approach to broaden the application of curcumin in the clinic in the near future.

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<p>Curcumin Affects Gastric Cancer Cell Migration, Invasion and Cytoskeletal Remodeling Through Gli1-β-Catenin</p>

Cited by 33 publications

References 59 publications

Insights into the role of ERp57 in cancer

Insights into the role of ERp57 in cancer

Polychemotherapy with Curcumin and Doxorubicin via Biological Nanoplatforms: Enhancing Antitumor Activity

Nanoscale Formulations: Incorporating Curcumin into Combination Strategies for the Treatment of Lung Cancer

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