Ferulic acid decreases cell viability and colony formation while inhibiting migration of MIA PaCa-2 human pancreatic cancer cells in vitro

Fahrioğlu, Umut; Dodurga, Yavuz; Elmas, Levent; Seçme, Mücahit

doi:10.1016/j.gene.2015.10.061

Cited by 74 publications

(39 citation statements)

References 27 publications

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“…The apoptosis triggered by FA may be associated with caspase-3 activation, since a decrease of procaspase-3 accompanied with an increase of caspase-3 are discovered in MLTC-1 tumoral cells and TM-3 Leydig cells treated FA 14. The apoptosis is stimulated by the significantly increased expression of caspase-3 in FA treated MIA PaCa-2 pancreatic cancer cells 15. It is discovered that caspase-3 was up-regulated in T24 bladder cancer cells cultured with FA 16.…”

Section: Discussionmentioning

confidence: 96%

“…According to the function, Bcl-2 family has another category members, like Bax, which promote the apoptosis 19. FA induced an increased expression of Bax accompanied with a significant decreased expression of Bcl-2 in the MIA PaCa-2 cells 15. It is reported that FA could increase expression of Bax with concomitant decreased Bcl-2 in the photocarcinogenesis progress of male Swiss albino mice skin 20.…”

Section: Discussionmentioning

confidence: 99%

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Ferulic acid promoting apoptosis in human osteosarcoma cell lines

Zhang¹,

Wu²,

Yang³

2017

Pak J Med Sci

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Objective:To explore the promoting apoptosis and antitumor activities of ferulic acid (FA) in human osteosarcoma and its potential mechanism.Methods:The SaOS-2 and MG63 osteosarcoma cell lines were opted to experiment and these cells were, respectively, cultured with various concentrations of FA (0 μM, 10 μM, 20 μM, 40 μM) for 72 hours at 37°C. The viabilities of the FA treated cells were monitored by MTT. Apoptosis cells were evaluated using annexin V/PI by flow cytometry. Apoptosis proteins caspase-3, procaspase-3, Bcl-2 and Bax were detected by western blot. Expressions of apoptotic genes Bcl-2 and Bax were quantified by qPCR.Results:The cell viabilities were critically declined in the concentration-dependent manner in FA groups (P < 0.01). The apoptosis cells were increased proportionately with the concentration of FA (P < 0.05). The procaspase-3 protein contents, and Bcl-2 mRNA and protein contents were significantly decreased while caspase-3 protein contents, and Bax mRNA and protein contents were concomitantly increased in the concentration-dependent manner in FA groups (P < 0.05). The response to FA by the SaOS-2 osteosarcoma cell was similar with the MG63 osteosarcoma cell (P > 0.05).Conclusion:Ferulic acid could significantly descend osteosarcoma cell viability through the promoting apoptosis pathway in which FA activates both caspase-3 and Bax and inactivates Bcl-2.

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Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Ferulic acid promoting apoptosis in human osteosarcoma cell lines

Zhang¹,

Wu²,

Yang³

2017

Pak J Med Sci

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“…Reduction in the number of colonies formed in the coumaric acid treated HCT-15 (32) and HT-29 (51) against the untreated (105 and 154) at 72 h confirmed the anti-proliferative effects of these compounds [52]. Other phenolic acids that have shown to exhibit antiproliferative activity include: (a) Caffeic- and 5-caffeoylquinic acid that reduced the cell viability of HT-29 colorectal carcinoma cell line and HT-1080 fibrosarcoma cells at 96 h by modulating cell cycle stages [58, 59]; (b) Di-caffeoylquinic acid, isolated from sweet potato, which inhibited the proliferation of DLD-1 human colon cancer cells [39]; (c) Ferulic acid and p-Coumaric acid that were shown to inhibit the pancreatic cancer cell line MIA-Pa-Ca-2 [60]; (d) Gallic acid, which inhibited cervical carcinomas cells HeLa and HTB-35 and Jukart [61, 62]. Similarly, even the phenyl substituted cinnamic acids also exhibited significant cytotoxicity in HT-29, A-549, OAW-42, MDA-MB-231 and HeLa cell lines with IC 50 values of <60 μM [63].…”

Section: In Vitro Studiesmentioning

confidence: 99%

“…A separate study demonstrated that Ferulic acid could upregulate Bax and downregulate Bcl-2 to induce apoptosis in osteosarcoma cells [64]. Similarly, FA has induced the expression of Bax, caspase-3 and -9 in fibrosarcoma cells [60]. Elevated caspase-3 was also observed when breast cancer cells were treated with 4-(3,4,5-Trimethoxyphenoxy) benzoic acid [57].…”

Section: In Vitro Studiesmentioning

confidence: 99%

An overview on the role of dietary phenolics for the treatment of cancers

Anantharaju

Prathima

Vimalambike

et al. 2016

Nutr J

351

225

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Plant derived phenolic compounds have been shown to inhibit the initiation and progression of cancers by modulating genes regulating key processes such as: (a) oncogenic transformation of normal cells; (b) growth and development of tumors; and (c) angiogenesis and metastasis. Recent studies focusing on identifying the molecular basis of plant phenolics-induced cancer cell death have demonstrated down-regulation of: (a) oncogenic survival kinases such as PI3K and Akt; (b) cell proliferation regulators that include Erk1/2, D-type Cyclins, and Cyclin Dependent Kinases (CDKs); (c) transcription factors such as NF-kβ, NRF2 and STATs; (d) histone deacetylases HDAC1 and HDAC2; and (e) angiogenic factors VEGF, FGFR1 and MIC-1. Furthermore, while inhibiting oncogenic proteins, the phenolic compounds elevate the expression of tumor suppressor proteins p53, PTEN, p21, and p27. In addition, plant phenolic compounds and the herbal extracts rich in phenolic compounds modulate the levels of reactive oxygen species (ROS) in cells thereby regulate cell proliferation, survival and apoptosis. Furthermore, recent studies have demonstrated that phenolic compounds undergo transformation in gut microbiota thereby acquire additional properties that promote their biological activities. In vitro observations, preclinical and epidemiological studies have shown the involvement of plant phenolic acids in retarding the cancer growth. However, to date, there is no clinical trial as such testing the role of plant phenolic compounds for inhibiting tumor growth in humans. More over, several variations in response to phenolic acid rich diets-mediated treatment among individuals have also been reported, raising concerns about whether phenolic acids could be used for treating cancers. Therefore, we have made an attempt to (a) address the key structural features of phenolic acids required for exhibiting potent anti-cancer activity; (b) review the reported findings about the mechanisms of action of phenolic compounds and their transformation by gut microbiota; and (c) update the toxicological aspects and anti-tumor properties of phenolic compounds and extracts containing phenolic compounds in animals.

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“…It is clinically used to treat angina pectoris and hypertensive diseases in China. FA has also been shown to possess antioxidant (Srinivasan et al 2007) and anticancer (Dodurga et al 2015;Fahrioglu et al 2016) properties. Interestingly, FA has been implicated in a reaction with endogenous copper that leads to DNA damage, and ultimately cell death, in cancer cells (Sarwar et al 2015).…”

Section: Introductionmentioning

confidence: 99%

Ferulic acid impairs osteoclast fusion and exacerbates survival of mature osteoclasts

et al. 2016

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Elevated bone loss induced by osteoclasts is a critical and most commonly observed pathological complication during osteolytic diseases such as osteoporosis. Hence, attenuation of osteoclast formation or function is a classical therapeutic approach to regulate bone loss. In this study, we found that ferulic acid (FA), a natural compound potently inhibited osteoclast formation in human CD14? peripheral blood monocytes ex vivo with an IC 50 of 39 lM. Moreover, due to impaired differentiation of osteoclast progenitors, actin ring formation and bone resorption activity were also perturbed. Investigation of underlying molecular mechanisms revealed that FA inhibited the RANKLinduced expression of dendritic cell-specific transmembrane protein (DC-STAMP), a critical regulator of osteoclast fusion. In addition, expression of matrix metalloproteinase-9 (MMP-9) and cathepsin K, the key osteoclast specific lysosomal proteases involved in bone matrix resorption were severely aggravated by FA. A significant reduction in mature osteoclast numbers was detected in the presence of FA accompanied by increased caspase-3 activity and DNAfragmentation, a characteristic hallmark of apoptosis. Collectively, these results suggested that FA inhibited osteoclast fusion by suppressing the expression of DC-STAMP and induced apoptosis in mature osteoclasts by the caspase-3 pathway.

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Ferulic acid decreases cell viability and colony formation while inhibiting migration of MIA PaCa-2 human pancreatic cancer cells in vitro

Cited by 74 publications

References 27 publications

Ferulic acid promoting apoptosis in human osteosarcoma cell lines

Ferulic acid promoting apoptosis in human osteosarcoma cell lines

An overview on the role of dietary phenolics for the treatment of cancers

Ferulic acid impairs osteoclast fusion and exacerbates survival of mature osteoclasts

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