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Review
. 2024 Sep 20;103(38):e39752.
doi: 10.1097/MD.0000000000039752.

A review on antitumor effect of pachymic acid

Affiliations
Review

A review on antitumor effect of pachymic acid

Yubo Xiao et al. Medicine (Baltimore). .

Abstract

Poria cocos, also known as Jade Ling and Songbai taro, is a dry fungus core for Wolfiporia cocos, which is parasitic on the roots of pine trees. The ancients called it "medicine of four seasons" because of its extensive effect and ability to be combined with many medicines. Pachymic acid (PA) is one of the main biological compounds of Poria cocos. Research has shown that PA has various pharmacological properties, including anti-inflammatory and antioxidant. PA has recently attracted much attention due to its anticancer properties. Researchers have found that PA showed anticancer activity by regulating apoptosis and the cell cycle in vitro and in vivo. Using PA with anticancer drugs, radiotherapy, and biomaterials could also improve the sensitivity of cancer cells and delay the progression of cancer. The purpose of this review was to summarize the anticancer mechanism of PA by referencing the published documents. A review of the collected data indicated that PA had the potential to be developed into an effective anticancer agent.

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Conflict of interest statement

The author declare that they have no competing interests.

Figures

Figure 1.
Figure 1.
PA could induce apoptosis in cancer cells by regulating the intrinsic pathway, extrinsic pathway, ER stress, and JAK2/STAT3 pathway. PA could also promote apoptosis by altering MMP and upregulating the expression of DNA damage-related proteins. ATF = activating transcription factor, BAK = Bcl-2 antagonist killer 1, Bax = Bcl-2-associated X, Bcl-2 = B cell lymphoma-2, Bcl-XL = B-cell lymphoma-extra large, BID = BH3-interacting domain death agonist, c-FLIP = cellular FLICE (FADD-like IL-1beta-converting enzyme)-inhibitory protein, CHOP = C/EBP homologous protein, Cyt-c = cytochrome c, DICS = death-inducing signaling complex, ER = endoplasmic reticulum, Fas = factor-related apoptosis IRE1 = inositol-required protein 1, PA = pachymic acid, PARP = poly (ADP-ribose) polymerase, p-ATR = p-serine/threonine-protein kinase ATR, p-Chk = p-serine/threonine-protein kinase Chk, p-eIF2α = p-eukaryotic initiation factor 2α, PERK = protein kinase RNA like ER kinase, p-JAK = Janus kinase, p-STAT3 = p-signal transducer and activator of transcription 3, PUMA = p53-upregulated mediator of apoptosis, ROS = reactive oxygen species, TNFR = tumor necrosis factor receptor-1, TRAIL = tumor necrosis factor-related apoptosis-inducing ligand, XBP-1 = α-X-box binding protein.
Figure 2.
Figure 2.
PA could cause cancer cells to enter a cell cycle arrest by inhibiting cyclin E/CDK2, COX/β-catenin. PA inhibited AKT-ERK, and the inhibition of p21 was released. PA also promoted p53; p21 was increased to degrade cyclinD-CDK4/6. AKT-ERK = protein kinase B-extracellular signal-regulated kinase, CDK = cyclin-dependent kinases, COX-2 = cyclooxygenase-2, PA = pachymic acid.

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