Allicin suppresses the migration and invasion in cervical cancer cells mainly by inhibiting NRF2

Zhang, Qiu-Mei; Yang, Dongmei

doi:10.3892/etm.2018.7104

Cited by 30 publications

(39 citation statements)

References 32 publications

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“…By inhibiting the microtubule polymerization, allicin inhibited cell polarization and migration, and reduced cell division [45,46]. Its antiproliferative activity was increased in a dose-dependent manner against human cervical cancer cells [20], cholangiocarcinoma [15], lung adenocarcinoma [44] renal cell carcinoma [47], and ovarian cancer cells [48]. Furthermore, allicin acts as a good inhibitor of colony formation, as well as cell migration [15].…”

Section: Discussionmentioning

confidence: 99%

“…After washing with TBST, the membranes were incubated with secondary antibodies conjugated with horseradish peroxidase. The signals were detected after adding the chemiluminescence substrate (Invitrogen, Carlsbad, CA, USA) [8,20].…”

Section: Western Blotmentioning

confidence: 99%

“…Different papers have reported the antitumor effects and molecular mechanisms of allicin in suppressing the malignant phenotype of cervical cancer cells, mainly by inhibiting the expression of NRF2 [20]; inhibiting proliferation and invasion in vitro and in vivo via SHP-1-mediated STAT3 signaling in cholangiocarcinoma [15]; and inducing apoptosis through the activation of both intrinsic and extrinsic pathways in glioma cells [21].…”

Section: Introductionmentioning

confidence: 99%

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The Synergistic Antitumor Effect of 5-Fluorouracil Combined with Allicin against Lung and Colorectal Carcinoma Cells

et al. 2020

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5-fluorouracil (5-FU) is an anticancer drug used to inhibit the proliferation of many different tumor cells. Since severe events are associated with this compound, its combination with different anticancer drugs or adjuvants would allow the use of a significantly lower dose of 5-FU. In this study, we highlighted that the combination of allicin with 5-FU inhibited the cell migration and proliferation of colorectal and lung cancer cells. 5-FU inhibited cell growth with a similar inhibitory concentration for both normal and tumor cells (~200µM), while allicin showed different inhibitory concentrations. With an IC50 of 8.625 µM, lung cancer cells were the most sensitive to allicin. Compared to 5-FU and allicin single-agent treatments, the co-treatment showed a reduced viability rate, with p < 0.05. The morphological changes were visible on all three cell lines, indicating that the treatment inhibited the proliferation of both normal and tumor cells. We highlighted different cell death mechanisms—apoptosis for lung cancer and a non-apoptotic cell death for colorectal cancer. The synergistic antitumor effect of 5-FU combined with allicin was visible against lung and colorectal carcinoma cells. Better results were obtained when a lower concentration of 5-FU was combined with allicin than the single-agent treatment at IC50.

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Section: Discussionmentioning

confidence: 99%

Section: Western Blotmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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The Synergistic Antitumor Effect of 5-Fluorouracil Combined with Allicin against Lung and Colorectal Carcinoma Cells

et al. 2020

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“…Otherwise, having an anti-NF-jB therapeutic modality might result into unwanted effects. Nrf2 is responsible for migration and invasion in cancers of the cervix [406], and aggressiveness in various cancers, such as breast cancer [407,408], gastric cancer [409] and colorectal cancer [410], or responsible for drug resistance in glioma and melanoma [411].…”

Section: Caffeic Acid Phenethyl Ester (Cape)mentioning

confidence: 99%

NF-κB signaling and crosstalk during carcinogenesis

Brücher

Läng

Jamall

2019

4open

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Transcription factors (TFs) are proteins that control the transcription of genetic information from DNA to mRNA by binding to specific DNA sequences either on their own or with other proteins as a complex. TFs thus support or suppress the recruitment of the corresponding RNA polymerase. In general, TFs are classified by structure or function. The TF, Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), is expressed in all cell types and tissues. NF-κB signaling and crosstalk are involved in several steps of carcinogenesis including in sequences involving pathogenic stimulus, chronic inflammation, fibrosis, establishment of its remodeling to the precancerous niche (PCN) and transition of a normal cell to a cancer cell. Triggered by various inflammatory cytokines, NF-κB is activated along with other TFs with subsequent stimulation of cell proliferation and inhibition of apoptosis. The involvement of NF-κB in carcinogenesis provides an opportunity to develop anti-NF-κB therapies. The complexity of these interactions requires that we elucidate those aspects of NF-κB interactions that play a role in carcinogenesis, the sequence of events leading to cancer.

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“…Allicin (diallyl thiosulfonate) is a versatile sulfur‐containing organic compound, which is an important lipid‐soluble active ingredient extracted from garlic ( Allium sativum L.). Studies reported that allicin has anti‐inflammatory, bactericidal, antioxidative stress, immunemodulation, neuroprotective, and antitumor effects (Borlinghaus, Albrecht, Gruhlke, Nwachukwu, & Slusarenko, 2014; Haghi, Azimi, & Rahimi, 2017; Hirsch et al., 2000; Li et al., 2019; Seki, Ishikawa, & Okada, 2018; Zhang & Yang., 2019; Zou et al., 2016). However, the effect and mechanism of allicin on the sensitivity of CRC radiotherapy have not been confirmed.…”

Section: Introductionmentioning

confidence: 99%

Allicin enhances the radiosensitivity of colorectal cancer cells via inhibition of NF‐κB signaling pathway

Huang

et al. 2020

Journal of Food Science

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Radioresistance is an important factor affecting the radiotherapy effect of colorectal cancer (CRC). Allicin is a versatile sulfur‐containing organic compound extracted from garlic (Allium sativum L.), which has many pharmacological effects. However, the effect of allicin on the sensitivity of CRC radiotherapy has not been confirmed. The present study is to observe the radiosensitivity effects of allicin and to explore its mechanism in CRC radiotherapy. The proliferation inhibition effects of allicin combined with X‐ray radiotherapy in HCT116 cells were measured by growth curve of cell and colony formation assays. The cell apoptosis was detected by Hoechst 33258 nucleus staining assay. The migration ability of cells was detected by Transwell chamber migration assay. The animal model of CRC was established in BALB/c mice via transplantation of CT26 cell, and the radiosensitization effect of allicin on CRC was detected in vivo. The mRNA expressions of NF‐κB, IKKβ, and IκBα were analyzed by reverse transcription‐polymerase chain reaction (RT‐PCR). The protein expressions of NF‐κB, p‐NF‐κB, IKKβ, p‐IKKβ, IκBα, and p‐IκBα were detected by western blotting. Our results showed that allicin improves the sensitivity of X‐ray radiotherapy in CRC, and its mechanism may be associated with inhibition of NF‐κB signaling pathway. These findings suggest that allicin may be used as a potential sensitizer for tumor radiotherapy in the clinic.

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Allicin suppresses the migration and invasion in cervical cancer cells mainly by inhibiting NRF2

Cited by 30 publications

References 32 publications

The Synergistic Antitumor Effect of 5-Fluorouracil Combined with Allicin against Lung and Colorectal Carcinoma Cells

The Synergistic Antitumor Effect of 5-Fluorouracil Combined with Allicin against Lung and Colorectal Carcinoma Cells

NF-κB signaling and crosstalk during carcinogenesis

Allicin enhances the radiosensitivity of colorectal cancer cells via inhibition of NF‐κB signaling pathway

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