CAJ | 학술논문

目的研究短肽RGDSY-CTTHWGFTLC对乳腺癌MCF-7细胞的抗肿瘤能力，为开发更高效的肽类抗肿瘤药物奠定实验理论基础。方法（1）化学合成目标短肽RGDSY-CTTHWGFTLC（简称RGDSY-CTT），阳性对照肽CTTHWGFTLC（简称CTT），阴性对照肽STTHWGFTLS（简称STT）；（2）将MCF-7细胞接种于预涂布纤连蛋白的96孔板，与短肽共孵育2 h，检测RGDSY-CTT对MCF-7细胞粘附能力的影响；（3）将MCF-7细胞接种于预铺基质胶的Transwell小室，与短肽共孵育16 h，检测RGDSY-CTT对MCF-7细胞侵袭能力的影响；（4）与短肽共孵育12 h后，MTT法检测RGDSY-CTT对MCF-7细胞增殖能力的影响；（5）与短肽共孵育24 h后，PI染色流式法检测RGDSY-CTT对MCF-7细胞凋亡和细胞周期的影响。结果（1）短肽对MCF-7细胞粘附能力的影响：RGDSY-CTT在终浓度为50、100、200μg/ml时，MCF-7细胞的粘附率依次为85.1%、74.1%和63.8%，随着浓度升高，粘附率明显降低，且比CTT组下降更显著（P<0.05）；（2）短肽对MCF-7细胞侵袭能力的影响：RGDSY-CTT在终浓度为100、200μg/ml时，对MCF-7细胞的侵袭抑制率分别为41.8%和63.9%；两个浓度均有明显抑制（P<0.01）；但与CTT组比抑制无显著差异（P>0.05）；（3）短肽对MCF-7细胞增殖的影响：RGDSY-CTT在终浓度为50、100、200μg/ml时，MCF-7细胞的增殖率依次为98.8%、82.4%和63.0%，随着肽浓度升高，增殖率下降明显；在100、200μg/ml时增殖抑制能力比CTT更强（P<0.05）；（4）短肽对MCF-7细胞凋亡和细胞周期的影响：RGDSY-CTT处理组MCF-7细胞经流式法检测到凋亡峰，细胞周期阻滞发生在G0/G1期，占76.7%，显著高于CTT组、STT组及正常对照组（P<0.01）。结论 RGDSY-CTT能抑制乳腺癌细胞的侵袭能力，同时还具有抑制乳腺癌细胞粘附、增殖和诱导肿瘤细胞凋亡的能力。
목적연구단태RGDSY-CTTHWGFTLC대유선암MCF-7세포적항종류능력，위개발경고효적태류항종류약물전정실험이론기출。방법（1）화학합성목표단태RGDSY-CTTHWGFTLC（간칭RGDSY-CTT），양성대조태CTTHWGFTLC（간칭CTT），음성대조태STTHWGFTLS（간칭STT）；（2）장MCF-7세포접충우예도포섬련단백적96공판，여단태공부육2 h，검측RGDSY-CTT대MCF-7세포점부능력적영향；（3）장MCF-7세포접충우예포기질효적Transwell소실，여단태공부육16 h，검측RGDSY-CTT대MCF-7세포침습능력적영향；（4）여단태공부육12 h후，MTT법검측RGDSY-CTT대MCF-7세포증식능력적영향；（5）여단태공부육24 h후，PI염색류식법검측RGDSY-CTT대MCF-7세포조망화세포주기적영향。결과（1）단태대MCF-7세포점부능력적영향：RGDSY-CTT재종농도위50、100、200μg/ml시，MCF-7세포적점부솔의차위85.1%、74.1%화63.8%，수착농도승고，점부솔명현강저，차비CTT조하강경현저（P<0.05）；（2）단태대MCF-7세포침습능력적영향：RGDSY-CTT재종농도위100、200μg/ml시，대MCF-7세포적침습억제솔분별위41.8%화63.9%；량개농도균유명현억제（P<0.01）；단여CTT조비억제무현저차이（P>0.05）；（3）단태대MCF-7세포증식적영향：RGDSY-CTT재종농도위50、100、200μg/ml시，MCF-7세포적증식솔의차위98.8%、82.4%화63.0%，수착태농도승고，증식솔하강명현；재100、200μg/ml시증식억제능력비CTT경강（P<0.05）；（4）단태대MCF-7세포조망화세포주기적영향：RGDSY-CTT처리조MCF-7세포경류식법검측도조망봉，세포주기조체발생재G0/G1기，점76.7%，현저고우CTT조、STT조급정상대조조（P<0.01）。결론 RGDSY-CTT능억제유선암세포적침습능력，동시환구유억제유선암세포점부、증식화유도종류세포조망적능력。
Objective To study the effect of the synthetic peptide RGDSY-CTTHWGFTLC on the biological behavior of breast cancer MCF-7 cells in vitro. Methods MCF-7 cells were incubated with different concentrations of the synthesized peptide RGDSY-CTTHWGFTLC (RGDSY-CTT), the positive control peptide CTTHWGFTLC (CTT), or the negative control peptide STTHWGFTLS (STT) in fibronectin-coated 96-well plates for different time lengths, and the changes in cell adhesion, invasiveness, proliferation, apoptosis and cell cycle were detected using Transwell chamber assay, MTT assay, and flow cytometry. Results Incubation of the cells with 50, 100 and 200 μg/ml of RGDSY-CTT caused a significant concentration-dependent inhibition of the cell adhesion (cell adhesion rates of 85.1%, 74.1% and 63.8%, respectively) with stronger effects than CTT (P<0.05). At 100 and 200μg/ml, RGDSY-CTT significantly inhibited the invasion (with inhibition rate of 41.8%and 63.9%, respectively) of MCF-7 cells with an effect similar to that by CTT (P>0.05). At 50, 100 and 200 μg/ml, RGDSY-CTT concentration-dependently suppressed MCF-7 cell proliferation (with cell proliferation rates of 98.8%, 82.4% and 63.0%, respectively), and this inhibitory effect was stronger than that of CTT at 100 and 200 μg/ml (P<0.05). The results of flow cytometry also demonstrated a stronger apoptosis-inducing effect of RGDSY-CTT (76.7%) than that in CTT, STT and the blank control groups (P<0.05). Conclusions RGDSY-CTT can inhibit cell invasion, suppress adhesion and proliferation, and induce apoptosis in MCF-7 cells.