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Review
. 2022 Mar 10:12:860508.
doi: 10.3389/fonc.2022.860508. eCollection 2022.

Therapeutic Implications of Caffeic Acid in Cancer and Neurological Diseases

Affiliations
Review

Therapeutic Implications of Caffeic Acid in Cancer and Neurological Diseases

Manzar Alam et al. Front Oncol. .

Abstract

Caffeic acid (CA) is found abundantly in fruits, vegetables, tea, coffee, oils, and more. CA and its derivatives have been used for many centuries due to their natural healing and medicinal properties. CA possesses various biological and pharmacological activities, including antioxidant, anti-inflammatory, anticancer, and neuroprotective effects. The potential therapeutic effects of CA are mediated via repression and inhibition of transcription and growth factors. CA possesses potential anticancer and neuroprotective effects in human cell cultures and animal models. However, the biomolecular interactions and pathways of CA have been described highlighting the target binding proteins and signaling molecules. The current review focuses on CA's chemical, physical, and pharmacological properties, including antioxidant, anti-inflammatory, anticancer, and neuroprotective effects. We further described CA's characteristics and therapeutic potential and its future directions.

Keywords: caffeic acid; clinical trials; diabetic neuropathy; inflammatory diseases; inhibitors; targeted therapy.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
A summary of connection among inflammation, cancer progression, and inhibitory action of CA. Many modulators involve inflammation in tumor progression. CA binds with modulators and represses cancer progression and stimulates apoptosis. [Adapted from Murtaza et al. (115) and Alam et al. (116)].
Figure 2
Figure 2
CA’s synergistic action with other agents/drugs (neuroprotective) for inhibiting neurodegeneration. [Adapted from Maity et al. (228)]. This figure was drown by ChemBioDraw.
Figure 3
Figure 3
Interaction of ERK2 with caffeic acid; hydrogen bonding between DHC O4’-D106, M108, and CA O3’-Q105 imparting molecular level inhibition of the protein [Adapted from Yang et al. (23)].
Figure 4
Figure 4
Molecular targets of caffeic acid. CA binds with Fyn for blocking its kinase activity and UV-mediated skin cancer. CA binds with MEK and TOPK to prevent their kinase actions and neoplastic cell transformation. [Adapted from Bode et al. (245)]. This figure was drown by ChemBioDraw.

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