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ISSN : 1225-1577(Print)
ISSN : 2384-0900(Online)
The Korean Journal of Oral and Maxillofacial Pathology Vol.49 No.6 pp.135-142
DOI : https://doi.org/10.17779/KAOMP.2025.49.6.002

Sargassum pallidum Extract Inhibits OSCC Growth through DNA Damage and Apoptosis Induction in Vitro

So-jung Jo1, Yedam Han2, Wook-Chul Kim3, Seung-Hong Lee4, Jongho Choi1, Sangshin Lee1*
1Department of Oral Pathology, College of Dentistry, Gangneung-Wonju National University
2Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University
3Department of Medical Science, Soonchunhyang University
4Department of Pharmaceutical Engineering, Soonchunhyang University

† These authors contributed equally to this work.


* Correspondence: Sangshin Lee, Department of Oral Pathology, College of Dentistry Gangneung-Wonju National University, 7Jukheon-gil, Gangneung-si, Gangwon-do, Korea Tel: +82-33-640-2468 Email: sangshin@gwnu.ac.kr ORCID: 0000-0002-6819-1486
November 20, 2025 December 4, 2025 December 26, 2025

Abstract


This study investigated the anticancer efficacy and underlying mechanism of Sargassum pallidum (S. pallidum) extract and evaluated its potential as a natural therapeutic candidate against oral squamous cell carcinoma (OSCC). To assess its cytotoxic and antiproliferative effects, human OSCC cell lines were treated with varying concentrations of S. pallidum extract. The extract significantly inhibited cell viability and proliferation in a dose-dependent manner. Moreover, treatment with S. pallidum extract induced DNA damage, evidenced by increased γH2AX protein expression and nuclear foci formation. This DNA damage subsequently triggered apoptosis, as indicated by increased levels of the proapoptotic protein Bak and decreased levels of the antiapoptotic protein BCL-2. Furthermore, terminal deoxynucleotidyl transferase dUTP nick-end labeling assay results confirmed apoptotic DNA fragmentation following treatment. Collectively, these findings demonstrate that S. pallidum extract suppresses OSCC cell viability and proliferation by inducing DNA damage–mediated apoptosis, highlighting its potential as a natural anticancer agent in OSCC therapy.


Sargassum pallidum , Oral squamous cell carcinoma , Chemotherapy , Proliferation , DNA damage , Apoptosis

시험관 내 큰잎알쏭이모자반 추출물의 DNA 손상 및 세포 사멸 유도를 통한 구강 편평세포 암종의 성장 억제 능력

조소정1, 한예담2, 김욱철3, 이승홍4, 최종호1, 이상신1*
1국립강릉원주대학교 치과대학 구강병리학교실
2연세대학교 생명시스템대학 생명공학과
3순천향대학교 의료과학대학
4순천향대학교 의약공학과

초록

    Ⅰ. INTRODUCTION

    Oral squamous cell carcinoma (OSCC) arises from the oral mucosa and represents one of the most prevalent malignancies of the head and neck region[1]. Tobacco use, excessive alcohol consumption, and genetic factors are recognized as major etiological contributors to OSCC. However, the precise molecular mechanisms underlying the pathogenesis of OSCC remain unclear[2]. According to the Global Cancer Observatory (GCO), approximately 377,713 new OSCC cases were diagnosed worldwide in 2020[3]. This disease is particularly prevalent in Asian countries and occurs more frequently in men than in women, particularly among middle-aged and elderly individuals[4]. OSCC often causes severe facial disfigurement and functional impairment, including dysphagia, speech difficulties, and loss of taste, leading to a significant decline in quality of life[5]. Current treatments for OSCC primarily involve a combination of surgery, radiotherapy, and chemotherapy[6]. Although surgical excision is effective for tumor removal, it frequently compromises essential oral functions such as chewing, swallowing, and speaking[7]. Similarly, radiotherapy lacks tissue specificity and may damage the surrounding normal tissues, and the nonspecific cytotoxicity of chemotherapeutic agents often leads to systemic side effects[8, 9]. Moreover, prolonged chemotherapy can induce drug resistance and reduce treatment efficacy[10]. These limitations underscore the urgent need for alternative therapeutic strategies that are both effective and less toxic.

    Natural marine products have emerged as promising sources of bioactive compounds for cancer therapy due to their unique chemical diversity and biological activities[11, 12]. Sargassum pallidum (S. pallidum), a brown seaweed widely distributed along the warm coastal regions of China, Japan, and Korea, has long been used in traditional Chinese medicine for the treatment of tumors[13]. Recent pharmacological studies have demonstrated that polysaccharides extracted from S. pallidum exhibit potent antioxidant, antibacterial, antiinflammatory, and anticancer properties[13-16]. Despite these findings, the precise molecular mechanisms underlying its antitumor effects remain unclear.

    Therefore, this study aimed to investigate the anticancer effects of S. pallidum extract on OSCC, elucidate the underlying mechanisms of action, and assess its potential as a natural therapeutic agent with reduced toxicity. Our findings provide new insights into the therapeutic potential of S. pallidum as a bioderived compound for the treatment of oral cancer.

    Ⅱ. MATERIALS and METHODS

    1. Cell lines and cell culture

    HSC-2 OSCC cells were cultured in Dulbecco’s Modified Eagle’s Medium (DMEM; Invitrogen, Carlsbad, CA, USA) supplemented with 10% fetal bovine serum (FBS; Gibco, Waltham, MA, USA) and 1% penicillin/streptomycin (P/S; Gibco). Cells were maintained at 37 °C in a humidified incubator containing 5% CO₂ (Thermo Fisher Scientific, Waltham, MA, USA). For experimental treatments, HSC-2 cells were incubated with S. pallidum extract at a final concentration of 170 μg/mL for 24 hours.

    2. Quantitative real-time polymerase chain reaction (qRT-PCR)

    Total RNA was extracted using TRIzol reagent (Invitrogen) according to the manufacturer’s instructions. RNA purity and concentration were determined spectrophotometrically, and cDNA synthesis was performed using the AccuPower RocketScript Cycle RT PreMix kit (Bioneer, Daejeon, South Korea; Cat. no. K-2101). Reverse transcription was performed at 50 °C for 60 minutes, followed by enzyme inactivation at 95 °C for 5 minutes. qRT-PCR was performed using AccuPower 2X GreenStar qPCR Master Mix (Bioneer) and a CFX96 Real-Time PCR Detection System (Bio-Rad Laboratories, Hercules, CA, USA). The cycling protocol consisted of 40 cycles at 95 °C for 15 seconds and 60 °C for 60 seconds. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) served as the internal reference gene, and relative expression levels were calculated using the 2⁻ΔΔCt method. Primer sequences were as follows: Bak: forward 5′-GGG AGA ACA GGG TAC GAT AA-3′, reverse 5′-GTC TGT CTG TGT GTG TGA TG-3′; GAPDH: forward 5′-CAA AGT TGT CAT GGA TGA CC-3′, reverse 5′-CCA TGG AGA AGG CTG GGG-3′.

    3. Western blot assay

    HSC-2 cells (3 × 10⁵) were seeded in 60-mm culture dishes and incubated for 24 hours before treatment with S. pallidum extract for additional 24 hours. Cells were lysed using 1× Laemmli buffer (Bio-Rad Laboratories) containing a protease inhibitor cocktail (Roche Diagnostics, Basel, Switzerland). Proteins were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and transferred onto 0.45-μm nitrocellulose membranes (GenDEPOT, Houston, TX, USA) for 16 hours. Membranes were blocked with 5% bovine serum albumin (BSA; Sigma-Aldrich, Burlington, MA, USA) for 30 minutes at room temperature and incubated overnight at 4 °C with primary antibodies: anti-Bak (1:1000; Santa Cruz Biotechnology, Dallas, TX, USA; Cat. no. sc-517390), anti- Bcl-2 (1:1000; Santa Cruz Biotechnology) and anti-GAPDH (1:3000; AbFrontier, Seoul, South Korea; Cat. no. LE-PA0018) as an internal control. After washing with phosphate-buffered saline (PBS) containing 0.1% Tween-20 (PBS-T), membranes were incubated with horseradish peroxidase (HRP)-conjugated secondary antibodies (goat anti-rabbit or anti-mouse IgG; 1:5000; Cell Signaling Technology, Danvers, MA, USA) for 1 hour at room temperature. Protein bands were visualized using an enhanced chemiluminescent (ECL) reagent (Millipore, Burlington, MA, USA) and imaged using a FUSION Solo S imaging system (Vilber, Eberhardzell, Germany). The band intensity was quantified using ImageJ software.

    4. Immunofluorescence

    HSC-2 cells were seeded on coverslips in 30-mm culture dishes at a density of 5 × 10⁴ cells and incubated overnight at 37 °C in 5% CO₂. Cells were treated with S. pallidum extract for 24 hours, fixed with 4% paraformaldehyde (PFA) for 30 minutes, and permeabilized with 0.5% Triton X-100 for 30 minutes at room temperature. Coverslips were incubated with an anti-γH2AX primary antibody (1:100; Cell Signaling Technology) for 1 hour at room temperature, followed by Alexa Fluor 488-conjugated secondary antibody (Invitrogen) for 1 hour in the dark. Nuclei were counterstained with 4′,6-diamidino-2-phenylindole (DAPI; Abcam, Cambridge, UK), and coverslips were mounted. Fluorescent images were acquired using a STELLARIS 5 confocal laser-scanning microscope (Leica Microsystems, Wetzlar, Germany) at 63× magnification. Three random fields per sample were analyzed using ImageJ software.

    5. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetr azolium bromide (MTT) assay

    The cytotoxicity of S. pallidum extract was evaluated using an MTT assay. HSC-2 cells (2.5 × 10³ cells/well) were seeded in 96-well plates and incubated for 24 hours at 37 °C in 5% CO₂. Cells were then treated with S. pallidum extract at concentrations ranging from 100 μg/mL to 500 μg/mL for 24 hours. The MTT solution (5 mg/mL; Sigma-Aldrich) was added to each well and incubated for 4 hours. Formazan crystals were dissolved in dimethyl sulfoxide for 30 minutes at room temperature. The absorbance was measured at 565 nm using a SpectraMax iD3 microplate reader (Molecular Devices, San Jose, CA, USA).

    6. 5-Ethynyl-2′-deoxyuridine (EdU) assay

    Cell proliferation was assessed using a Click-iT Plus EdU Alexa Fluor 488 Assay Kit (Invitrogen; Cat. no. C10337), according to the manufacturer’s protocol. HSC-2 cells (5 × 10⁴) were seeded on coverslips in 30-mm dishes and incubated for 24 hours before treatment with S. pallidum extract. After 24 hours, 2 μg/mL EdU solution was added, then the cells were incubated for 2 hours. Subsequently, the cells were fixed with 4% PFA for 30 minutes, permeabilized with 0.5% Triton X-100, and stained with Click-iT reaction cocktail for 30 minutes at room temperature. Nuclei were counterstained with DAPI (Abcam) and imaged using an Olympus BX53 fluorescence microscope (20× objective; Olympus Corporation, Tokyo, Japan). EdU-positive cells were quantified using ImageJ software.

    7. Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay

    Apoptotic DNA fragmentation was assessed using the In Situ Cell Death Detection Kit TMR Red (Roche Diagnostics) according to the manufacturer’s protocol. HSC-2 cells (5 × 10⁴) were seeded on coverslips, incubated overnight, and treated with S. pallidum extract for 24 hours. The cells were fixed with 4% PFA for 30 minutes and permeabilized with 0.5% Triton X-100 for 30 minutes at room temperature. After washing with Dulbecco's Phosphate-Buffered Saline, samples were incubated with the TUNEL reaction mixture for 2 hours in the dark. After counterstaining with DAPI, images were acquired using an Olympus fluorescence microscope (20× objective; Olympus Corporation, Tokyo, Japan). Three random fields were analyzed, and TUNEL-positive cells were quantified using ImageJ software.

    8. Statistical analysis

    All experiments were independently repeated three times. Data are expressed as mean ± standard error of the mean (SEM). Statistical significance between control and treatment groups was determined using an unpaired Student’s t-test. Analyses and graph generation were performed using GraphPad Prism 9 software (GraphPad Software, San Diego, CA, USA). Statistical significance was set at a p-value <0.05.

    Ⅲ. RESULTS

    1. S. pallidum extract inhibited cell viability and proliferation in HSC-2 cells

    To evaluate the cytotoxic effect of S. pallidum extract, an MTT assay was performed. Treatment with S. pallidum extract significantly reduced the viability of HSC-2 cells in a concentration-dependent manner, with an IC₅₀ value of 170 μg/mL (Fig. 1A). Furthermore, the EdU incorporation assay, which measures DNA synthesis, revealed a marked decrease in the number of EdU-positive cells in the S. pallidum- treated group compared with that in the control group. These findings indicate that S. pallidum extract effectively suppressed the growth and proliferation of OSCC cells (Fig. 1B).

    2. S. pallidum extract induced DNA damage in HSC-2 cells

    To elucidate the mechanism underlying the reduced cell viability caused by S. pallidum extract, we examined DNA damage in HSC-2 cells. Western blot analysis showed that the expression of γH2AX, a well-established marker of DNA double-strand breaks (DSBs), was markedly elevated in S. pallidum–treated cells compared with that in the control group (Fig. 2A). In addition, immunofluorescence staining revealed a significant increase in γH2AX foci formation in the nuclei of treated HSC-2 cells, confirming that S. pallidum extract induced substantial DNA damage (Fig. 2B).

    3. S. pallidum extract promoted apoptosis in HSC-2 cells

    Previous studies have reported that S. pallidum extract induces apoptosis in various cancer cell types[13]. Consistent with these findings, our results demonstrated that S. pallidum extract promoted apoptotic cell death in OSCC cells. Western blot analysis revealed increased expression of Bak and decreased expression of the antiapoptotic marker BCL-2 (Fig. 3A). Increased Bak expression was also confirmed by the qRT-PCR analysis (Fig. 3B). Furthermore, the TUNEL assay results confirmed a significant increase in the number of TUNEL-positive cells following S. pallidum treatment (Fig. 3C).

    Ⅳ. DISCUSSION

    OSCC is one of the most prevalent life-threatening malignancies worldwide[17]. Despite advances in multimodal treatments, including surgery, radiotherapy, and cisplatin-based chemotherapy, therapeutic outcomes remain limited, and these conventional therapies often result in severe side effects that negatively impact patients’ quality of life[3]. Among these adverse effects, oral mucositis is frequently observed in patients with OSCC receiving chemotherapy or radiotherapy and is a major complication that impairs oral function, hinders nutritional intake, and compromises treatment continuity, thereby reducing clinical efficacy[18]. Moreover, the frequent emergence of chemoresistance further diminishes the effectiveness of anticancer drugs, often leading to tumor recurrence and metastasis[19]. Therefore, there is growing interest in developing natural product–based anticancer agents that can overcome these therapeutic limitations by offering reduced toxicity and improved safety.

    S. pallidum, a brown marine alga, has long been consumed as food and utilized in traditional medicine in East Asia, indicating a relatively high level of safety[20]. These characteristics make it an appealing candidate for cancer therapy, as it may circumvent the systemic toxicity and organ damage frequently observed with conventional chemotherapy. In the present study, we demonstrated that S. pallidum extract exerts anticancer effects against OSCC cells by inducing DNA double-strand breaks (DSBs) and promoting apoptosis. Notably, γH2AX accumulation and TUNEL-positive apoptotic nuclei were observed following treatment, suggesting S. pallidum induces DSB-mediated cell death similar to that seen with established chemotherapeutic agents such as doxorubicin[21]. This finding indicates that S. pallidum exerts genotoxic stress capable of triggering apoptosis, thereby suppressing OSCC cell survival and proliferation. In addition, the increased expression of proapoptotic markers, such as Bak, together with the decreased expression of antiapoptotic BCL-2, further supports the proapoptotic activity of S. pallidum extract. These results are consistent with those of previous studies that reported marine- derived polysaccharides can modulate apoptotic pathways through mitochondrial dysfunction and reactive oxygen species generation[13, 16]. Thus, S. pallidum is a promising natural modulator of apoptosis in OSCC cells. However, this study had some limitations. First, only one OSCC cell line (HSC-2) was used, limiting the generalizability of our findings. Future studies should include multiple OSCC cell lines to verify the consistency of the observed effects. Second, although S. pallidum is considered a safe traditional food source, toxicological studies on normal oral cells and in vivo models are necessary to assess its selective cytotoxicity toward cancer cells. Finally, because the extract contains a mixture of bioactive compounds, the identification and isolation of specific active components responsible for the observed anticancer effects are required to elucidate the precise molecular mechanisms and therapeutic potential.

    In summary, our findings suggest that S. pallidum extract exerts anticancer effects against OSCC by inducing DNA damage and apoptosis, providing a scientific basis for its potential development as a next-generation natural therapeutic agent. Further biosafety, mechanistic, and compound purification studies are crucial to validate its clinical applicability and to establish S. pallidum as a viable alternative or adjunct to existing chemotherapeutic regimens.

    ACKNOWLEDGMENTS

    This study was supported by the National Research Foundation of Korea (RS-2024-00458489, RS-2025-00519106) and 2025 academic research support program in Gangneung- Wonju National University.

    Figure

    KAOMP-49-6-135_F1.jpg

    S. pallidum extract (SPE) was shown to suppress HSC-2 cells proliferation. (a) The cytotoxicity of SPE was evaluated using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. HSC-2 cells were treated with various concentrations of S. pallidum extract (0, 100, 200, 300, 400, and 500 μg/mL) for 24 hours. (b) Cell proliferation was measured using a 5-ethynyl-2′-deoxyuridine (EdU) assay. Blue fluorescence indicated the nuclei, and green fluorescence within cells indicated normal cell proliferation. The graph was created after randomly photographing three areas and counting EdU positive cells. Scale bar: 50 μm. Magnification: 20×. * p < 0.05. All experiments were independently repeated at least three times to ensure reproducibility.

    KAOMP-49-6-135_F2.jpg

    S. pallidum extract (SPE) was shown to induce DNA double strands break in HSC-2 cells. (a) Western blot analysis showed the protein level of γH2AX in HSC-2 cells treated with S. pallidum extract. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) was used as the internal control. The graph shows the relative intensity of each protein band measured using imageJ software. (b) Confocal immunofluorescence was used to analyze the γH2AX foci in HSC-2 cells treated with S. pallidum extract. Blue fluorescence indicated the nuclei, and green fluorescence indicated expression of γH2AX. The graph was created after randomly photographing three areas and counting γH2AX foci. Scale bar: 20 μm. Magnification: 63×. * p < 0.05. All experiments were independently repeated at least three times to ensure reproducibility.

    KAOMP-49-6-135_F3.jpg

    Sargassum pallidum (S. pallidum) extract was shown to induce apoptotic cell death in HSC-2 cells. (a) Western blot analysis showed the protein levels of Bak and BCL-2 in HSC-2 cells treated with S. pallidum extract. Glyceraldehyde 3-phosphate dehydrogenase (GAPDH) was used as the internal control. The graph shows the relative intensity of each protein band measured using imageJ software. (b) The relative mRNA expression levels of Bak in HSC-2 cells treated with S. pallidum extract are shown. Gene expression was quantified using quantitative real-time polymerase chain reaction (qRT-PCR) and normalized to GAPDH. (c) DNA fragmentation and apoptosis were detected using a terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. Blue fluorescence indicated the nuclei, and red fluorescence indicated DNA fragmentation and apoptosis. The graph was created after randomly photographing three areas and counting TUNEL-positive cells, expressed as a percentage. Scale bar: 50 μm. Magnification: 20×. *p < 0.05. All experiments were independently repeated at least three times to ensure reproducibility.

    Table

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