Palmitic acid (PA) is a saturated fatty acid commonly found in coconut oil and palm oil. It serves as an energy source for the body and plays a role in the structure and function of cell membranes. Beyond its industrial applications, PA has gained attention for its potential therapeutic properties. Modern pharmacological studies have demonstrated that PA exhibits anti-inflammatory, antioxidant, and immune-enhancing effects. In recent years, PA has emerged as a promising anti-tumor agent with demonstrated efficacy against various malignancies including gastric cancer, liver cancer, cervical cancer, breast cancer, and colorectal cancer. Its anti-tumor effects encompass inducing apoptosis in tumor cells, inhibiting tumor cell proliferation, suppressing metastasis and invasion, enhancing sensitivity to chemotherapy, and improving immune function. The main anticancer mechanism of palmitic acid (PA) involves the induction of cell apoptosis through the mitochondrial pathway, facilitated by the promotion of intracellular reactive oxygen species (ROS) generation. PA also exhibits interference with the cancer cell cycle, leading to cell cycle arrest predominantly in the G1 phase. Moreover, PA induces programmed cell autophagy death, inhibits cell migration, invasion, and angiogenesis, and synergistically enhances the efficacy of chemotherapy drugs while reducing adverse reactions. PA acts on various intracellular and extracellular targets, modulating tumor cell signaling pathways, including the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt), endoplasmic reticulum (ER), B Cell Lymphoma-2 (Bcl-2), P53, and other signaling pathways. Furthermore, derivatives of PA play a significant regulatory role in tumor resistance processes. This paper provides a comprehensive review of recent studies investigating the anti-tumor effects of PA. It summarizes the underlying mechanisms through which PA exerts its anti-tumor effects, aiming to inspire new perspectives for the treatment of malignant tumors in clinical settings and the development of novel anti-cancer drugs. 

Molecular mechanism of palmitic acid and its derivatives in tumor progression

GC-MS Analysis of Persicaria bistorta: Uncovering the Molecular Basis of Its Traditional Medicinal Use.

Oral squamous cell carcinoma (OSCC) is one of the most common human malignancies worldwide. The molecular mechanisms of OSCC pathogenesis are still unknown; however, in recent years, several reports have focused on the role of enhancer of zeste homolog 2 (EZH2) in OSCC. Therefore, in this study we aimed to investigate the effects of GSK343, a selective EZH2 inhibitor, and its impact on the signaling pathways in OSCC, using an in vitro and in vivo orthotopic model. In the in vitro model, GSK343 (1, 10, and 25 μM) significantly decreased OSCC cell viability and cell migration through EZH2 inhibition, modulating NF-κB/IκBα pathway activation and eNOS, VEGF, and TGFβ expression, important markers of angiogenesis. In the in vivo model, GSK343 (5 mg/kg and 10 mg/kg) restored tongue tissue architecture and reduced tumor progression through EZH2 inhibition and Wnt/β-catenin signaling pathway modulation. Moreover, GSK343 reduced the expression of inflammatory mediators; eNOS and TGFβ, markers of angiogenesis; and CD31 and CD34, markers of micro vessel density, respectively. In conclusion, our data demonstrate that GSK343 counteracts oral cancer progression through EZH2/Wnt/β-catenin pathway modulation, suggesting that it could be a promising therapeutic approach for OSCC management. 

EZH2 Inhibition to Counteract Oral Cancer Progression through Wnt/β-Catenin Pathway Modulation

Natural volatile organic compounds (VOCs) obtained from five Rubiaceae plants native to south China, namely Damnacanthus indicus, Hamelia patens, Exallage chrysotricha, Psychotria serpens, and Spermacoce pusilla, were isolated and characterized in this study. The analysis revealed that each plant contained 71, 57, 80, 73, and 70 volatile organic chemical compounds, respectively. The main VOCs shared by five plants was palmitate (10.20%–36.26%). Methyl salicylate, caryophyllene oxide, tetradecanoic acid, 6,10,14-trimethyl-2-pentadecanone, pentadecanoic acid, pentacosane, pentadecanal, nonanal, hexadecanoic acid methyl ester, phytol, linalool, and (E)-β-ionone were shared by at least 4 Rubiaceae plants in this study. Besides, each of the five plants has its main components as follows: 12.81% ethyl linoleate and 6.13% (E)-13-octadecenoic acid for D. indicus; 35.17% methyl salicylate for H. patens; 9.50% (Z, Z)-9,12-octadecadienoic acid and 7.56% endo-borneol for E. chrysotricha; 13.93% methyl salicylate for P. serpens; 6.19% humulene and 6.08% humulene oxide II for S. pusilla. This research provides insights into the phytochemical diversity and classification of Rubiaceae plants, laying a solid foundation for future natural product development in the Rubiaceae family. 

Volatile organic composition of five Rubiaceae species: Insights into their phytochemical diversity

MicroRNAs (miRNAs) can regulate several physiological processes of cells after transcription, such as cell proliferation, differentiation, and apoptosis. In this study, we found that 500 μM of palmitic acid (PA) could significantly induce the apoptosis of porcine subcutaneous preadipocytes (p < 0.05). The overexpression of miR‐429 decreased the apoptotic rate of porcine preadipocytes and inhibited the expression of the proapoptotic gene P53 (p < 0.05). In addition, miR‐429 can specifically bind to the 3′ untranslated region of Sox5, and the upregulation of miR‐429 downregulated Sox5 expression. However, Sox5 overexpression promoted the apoptosis of porcine preadipocytes (p < 0.01); the co‐transfection of miR‐429 and pcDNA3.1‐Sox5 into preadipocytes could reverse the inhibition of PA‐induced apoptosis by miR‐429. In conclusion, the present results provide a theoretical basis for elucidating the molecular mechanisms by which miR‐429 and Sox5 regulate the apoptosis of porcine subcutaneous preadipocytes.

miR‐429 inhibits palmitic acid‐induced apoptosis of porcine subcutaneous preadipocytes by targeting Sox5

OBJECTIVE
Despite apoptosis processes being conserved, cancer cells have developed mechanisms to inhibit apoptosis by altering anti-apoptotic molecules or inactivating pro-apoptotic. The aim of this study was to determine the palmitic acid of Musa paradisiaca var. sapientum (L) Kunz (MP) stem extracts against human oral squamous cell carcinoma (hOSCC) through caspase-3.


MATERIALS AND METHODS
Ethanol and ethyl acetate extracts of MP stem were analyzed by gas chromatography-mass spectrometry (GC-MS). Computerized models of chemically active compounds were used to predict anticancer activity. Cytotoxicity was evaluated in Artemia salina Leach and hOSCC (OM-1) culture at concentrations 100, 90, 80, 70, 60, 50, 40, 30, 20, and 10 µg/mL respectively. The expression level of caspase-3 on hOSCC was measured by enzyme-linked immunoassay (ELISA).


RESULTS
We found seven chemically active compounds in the ethanol extract and 15 compounds in the ethyl acetate extract of MP stem. The major component was hexadecanoic acid of palmitic acid derivates, and this was predicted to have anticancer activities as apoptosis through caspase-3 stimulants. However, cytotoxicity effects against hOSCC culture were assessed by values of the 50% inhibitory concentration (IC50) of 15.00 µg/mL for the ethanol extract, and an IC50 of 10.61 µg/mL for the ethyl acetate. There was a significant increase of caspase-3 level on treatment groups compared to control.


CONCLUSIONS
Hexadecanoic acid of MP stem extracts has anticancer activity by inhibiting cell growth of hOSCC culture through caspase-3 stimulants.

Palmitic acid of Musa Paradisiaca induces apoptosis through caspase-3 in human oral squamous cell carcinoma.

The advancements in the cell culture studies have led to the development of regenerative medicine concept. The aim of this study is to compare the effectiveness of some washing solutions, including phosphate buffered saline (PBS), sodium chloride (NaCl), and ringer's lactate (RL) on the rate of detachment and confluency in fibroblast and osteoblast cell culture. Baby Hamster Kidney 21 clone 13 (BHK21/C13) fibroblast cells and 7F2 osteoblast were cultured on T25 flasks for 3-4 days. Three treatment groups were classified on the basis of different washing solutions used in the moment before trypsinization: PBS, 0.9% NaCl, and RL. Each group was measured for the detachment rate and cell confluence. The measurement was done in 2 passage numbers. The use of PBS, NaCl, and RL washing solution showed that detachment time was less than 5 minutes for the fibroblasts and 3 minutes for the osteoblasts. There was a significant difference in the rate of fibroblast cell detachment (p=0.006) and osteoblast (p=0.016). The capability of fibroblasts and osteoblasts to achieve a confluence of 106 cells/well on the first and second measurements was almost the same between the washing solution groups. The use of physiological 0.9% NaCl solution as a washing solution in fibroblast and osteoblast cell culture has almost the same effectiveness as PBS to help accelerate cell detachment in less than 5 minutes without influencing the capability of cells to proliferate.

Cell detachment rates and confluence of fibroblast and osteoblast cell culture using different washing solutions.

A promising oral anticancer of hexadecanoic acid on genotoxicity evaluation of micronuclei and apoptosis induction.

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Palmitic acid of Musa Paradisiaca induces apoptosis through caspase-3 in human oral squamous cell carcinoma.

Cell detachment rates and confluence of fibroblast and osteoblast cell culture using different washing solutions.

A promising oral anticancer of hexadecanoic acid on genotoxicity evaluation of micronuclei and apoptosis induction.