ω-3 free fatty acids and all-trans retinoic acid synergistically induce growth inhibition of three subtypes of breast cancer cell lines

Lin, Guangxiao; Zhu, S. Y.; Wu, Yikuan; Song, Ci; Wang, Wanjing; Zhang, Yuan; Chen, Yue‐Lei; He, Zhao

doi:10.1038/s41598-017-03231-9

Cited by 32 publications

(38 citation statements)

References 56 publications

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“…Indeed, with EPA and DHA treatment for 3 days, downregulation of GPR120 by siRNA knockdown approach in breast cancer cells significantly increased cell growth inhibition in both MCF-7 and SKBR-3 cells but not MDA-MB-231 cells, indicating that v-3 PUFAs-induced breast cancer cell growth inhibition is independent of GPR120 receptor ( Figures 3A-1C). Furthermore, previous studies have revealed that v-3 PUFAs could inhibit mammary tumor progression via increasing cell apoptosis (Lin et al, 2017). To investigate whether GPR120 is also not involved in v-3 PUFAs-induced cell apoptosis.…”

Section: Gpr120 Is Not Involved In the Anti-tumor Effects Of V-3 Pufasmentioning

confidence: 99%

“…GPR120 was highly expressed in breast cancer cells and promoted breast cancer cell growth, however, which was opposite to the cell growth inhibitory effect of v-3 PUFAs in breast cancer cells. Furthermore, previous studies have revealed that v-3 PUFAs could inhibit mammary tumor progression via increasing cell apoptosis (Lin et al, 2017). Indeed, with EPA and DHA treatment for 3 days, downregulation of GPR120 by siRNA knockdown approach in breast cancer cells significantly increased cell growth inhibition in both MCF-7 and SKBR-3 cells but not MDA-MB-231 cells, indicating that v-3 PUFAs-induced breast cancer cell growth inhibition is independent of GPR120 receptor ( Figures 3A-1C).…”

Section: Gpr120 Is Not Involved In the Anti-tumor Effects Of V-3 Pufasmentioning

confidence: 99%

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GPR120 is not required for ω‐3 PUFAs‐induced cell growth inhibition and apoptosis in breast cancer cells

Zhu

Jiang

et al. 2017

Cell Biology International

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Intake of ω-3 PUFAs reduces the frequency of breast cancer, and GPR120 receptor transduces ω-3 PUFAs signaling to increase insulin sensitivity in mice, but whether GPR120 mediates ω-3 PUFAs signaling to inhibit breast carcinogenesis is currently unknown. In the present study, we found that GPR120 is highly expressed in human breast cancerous tissues but not adjacent normal tissue. Knockdown of GPR120 by siRNA in breast cancer cells significantly reduced cell growth, and dramatically increased ω-3 FFA-induced cell growth inhibition and apoptosis. Thus, these observations indicated that GPR120 promotes breast cancer cell growth, whereas ω-3 PUFA-induce breast cancer cell apoptosis independently of GPR120.

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Section: Gpr120 Is Not Involved In the Anti-tumor Effects Of V-3 Pufasmentioning

confidence: 99%

Section: Gpr120 Is Not Involved In the Anti-tumor Effects Of V-3 Pufasmentioning

confidence: 99%

GPR120 is not required for ω‐3 PUFAs‐induced cell growth inhibition and apoptosis in breast cancer cells

Zhu

Jiang

et al. 2017

Cell Biology International

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“…It has been largely reported that inflammation, recognized as a hallmark of cancer, is able to predispose tumor development and progression by well-orchestrated reciprocal interactions among cancer cells and surrounding stromal inflammatory cells within the tumor microenvironment. Several lines of evidence indicate that DHA and EPA, apart from their anti-inflammatory actions, have beneficial effects in cancer [76][77][78][79][80][81][82], suggesting their potential role either in cancer prevention or therapy. The main anti-neoplastic activities of n−3 PUFAs include the alteration of the composition of cell surface membrane and lipid raft disruption, the modulation of COX activity, the increased cellular oxidative stress, and the binding and activation of different receptors, including CBs, GPRs, TRVP1, and PPARs [83].…”

Section: N-acylserotonin Dha-5htmentioning

confidence: 99%

n–3 Polyunsaturated Fatty Acid Amides: New Avenues in the Prevention and Treatment of Breast Cancer

Giordano

Plastina

Barone

et al. 2020

IJMS

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Over the last decades a renewed interest in n−3 very long polyunsaturated fatty acids (PUFAs), derived mainly from fish oils in the human diet, has been observed because of their potential effects against cancer diseases, including breast carcinoma. These n−3 PUFAs mainly consist of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) that, alone or in combination with anticancer agents, induce cell cycle arrest, autophagy, apoptosis, and tumor growth inhibition. A large number of molecular targets of n−3 PUFAs have been identified and multiple mechanisms appear to underlie their antineoplastic activities. Evidence exists that EPA and DHA also elicit anticancer effects by the conversion to their corresponding ethanolamide derivatives in cancer cells, by binding and activation of different receptors and distinct signaling pathways. Other conjugates with serotonin or dopamine have been found to exert anti-inflammatory activities in breast tumor microenvironment, indicating the importance of these compounds as modulators of tumor epithelial/stroma interplay. The objective of this review is to provide a general overview and an update of the current n−3 PUFA derivative research and to highlight intriguing aspects of the potential therapeutic benefits of these low-toxicity compounds in breast cancer treatment and care.

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“…Cells were collected for fixation and stored at 4 • C prior to cell cycle analysis. The cells were then harvested with 70% ethanol, centrifuged, washed twice with PBS and then stained with a solution containing 100 µg/mL RNase A, 0.2% Triton X-100 and 50 µg/mL propidium iodide (Sigma-Aldrich, St. Louis, MO, USA) for 1 h at 4 • C in darkness before the cell cycle was measured with a flow cytometer within 1 h [39].…”

Section: Pi Staining Assaymentioning

confidence: 99%

Antiproliferation Activity and Mechanism of c9, t11, c15-CLNA and t9, t11, c15-CLNA from Lactobacillus plantarum ZS2058 on Colon Cancer Cells

et al. 2020

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Conjugated linolenic acid (CLNA) is a type of ω-3 fatty acid which has been proven to have a series of benefits. However, there is no study about the function of Lactobacillus-derived CLNA isomer. Lactobacillus plantarum ZS2058 has been proven to manifest comprehensive functions and can produce CLNA. To investigate the specific functions of CLNA produced by this probiotic bacterium, two different conjugated α-linolenic acid (CLNA) isomers were successfully isolated. These isoforms, CLNA1 (c9, t11, c15-CLNA, purity 97.48%) and CLNA2 (c9, t11, t15-CLNA, purity 99.00%), both showed the ability to inhibit the growth of three types of colon cancer cells in a time- and concentration-dependent manner. In addition, the expression of MDA in Caco-2 cells was increased by CLNA1 or CLNA2, which indicated that lipid peroxidation was related to the antiproliferation activity of CLNAs. An examination of the key protein of pyroptosis showed that CLNA1 induced the cleavage of caspase-1 and gasdermin-D, while CLNA2 induced the cleavage of caspase-4, 5 and gasdermin-D. The addition of relative inhibitors could alleviate the pyroptosis by CLNAs. CLNA1 and CLNA2 showed no effect on caspase-3, 7, 9 and PARP-1, which were key proteins associated with apoptosis. No sub-diploid apoptotic peak appeared in the result of PI single staining test. In conclusion, CLNA1 activated caspase-1 and induced Caco-2 cell pyroptosis, whereas CLNA2 induced pyroptosis through the caspase-4/5-mediated pathway. The inhibition of Caco-2 cells by the two isomers was not related to apoptosis. This is the first study on the function of Lactobacillus-derived CLNA isomer. The inhibition pathway of Lactobacillus-derived CLNA isomer on colon cancer cells were proved.

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ω-3 free fatty acids and all-trans retinoic acid synergistically induce growth inhibition of three subtypes of breast cancer cell lines

Cited by 32 publications

References 56 publications

GPR120 is not required for ω‐3 PUFAs‐induced cell growth inhibition and apoptosis in breast cancer cells

GPR120 is not required for ω‐3 PUFAs‐induced cell growth inhibition and apoptosis in breast cancer cells

n–3 Polyunsaturated Fatty Acid Amides: New Avenues in the Prevention and Treatment of Breast Cancer

Antiproliferation Activity and Mechanism of c9, t11, c15-CLNA and t9, t11, c15-CLNA from Lactobacillus plantarum ZS2058 on Colon Cancer Cells

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