Luo Qingbin, Zhu Bohui, Wang Cuilan, Wang Yiran
Department of Radiation Oncology, Anhui Zhongke Genjiu Hospital, 230051 Hefei, Anhui, China.
Department of Oncology, Shanghai Pudong New Area Gongli Hospital, 200135 Shanghai, China.
Discov Med. 2025 Jan;37(192):182-192. doi: 10.24976/Discov.Med.202537192.15.
Cytoskeleton-associated protein 2 like () has been demonstrated to mediate the cell cycle in cancer cells. However, it is unknown whether CKAP2L impacts colorectal cancer (CRC). The purpose of this study was to investigate the role of in CRC.
and regulatory factor X 5 () expression profiles in colon adenocarcinoma (COAD) and rectal adenocarcinoma (READ) were analyzed in UALCAN. Human colorectal adenocarcinoma epithelial cells, DLD1, were transfected with small interfering RNA targeting and -overexpressing vectors (OE-CKAP2L). The interaction between and was identified by dual-luciferase assay and chromatin immunoprecipitation. Epithelial-mesenchymal transition (EMT)- and protein kinase B/mammalian target of the rapamycin (AKT/mTOR) pathway-associated proteins were evaluated by western blotting.
and expression was increased in CRC based on the UALCAN database. downregulation inhibited proliferation, migration, invasion, and EMT while promoting G1/S phase arrest ( < 0.01). knockdown downregulated expression and mediated the inactivation of the AKT/mTOR pathway ( < 0.001). acted as an upstream transcription factor of . overexpression attenuated the restriction of downregulation on CRC cell malignant phenotypes ( < 0.01).
transcriptionally activated by accelerates CRC proliferation and metastasis by promoting the cell cycle and EMT. This study provides potential molecular targets for treating CRC.
细胞骨架相关蛋白2样蛋白(CKAP2L)已被证明可介导癌细胞的细胞周期。然而,CKAP2L是否影响结直肠癌(CRC)尚不清楚。本研究的目的是探讨CKAP2L在CRC中的作用。
在UALCAN中分析结肠腺癌(COAD)和直肠腺癌(READ)中CKAP2L和调控因子X5(RFX5)的表达谱。用靶向CKAP2L的小干扰RNA和过表达载体(OE-CKAP2L)转染人结肠腺癌上皮细胞DLD1。通过双荧光素酶测定和染色质免疫沉淀鉴定CKAP2L与RFX5之间的相互作用。通过蛋白质印迹法评估上皮-间质转化(EMT)和蛋白激酶B/雷帕霉素哺乳动物靶标(AKT/mTOR)通路相关蛋白。
基于UALCAN数据库,CRC中CKAP2L和RFX5的表达增加。CKAP2L下调抑制增殖、迁移、侵袭和EMT,同时促进G1/S期阻滞(P<0.01)。CKAP2L敲低下调RFX5表达并介导AKT/mTOR通路失活(P<0.001)。CKAP2L作为RFX5的上游转录因子。CKAP2L过表达减弱了CKAP2L下调对CRC细胞恶性表型的限制(P<0.01)。
RFX5由CKAP2L转录激活,通过促进细胞周期和EMT加速CRC增殖和转移。本研究为治疗CRC提供了潜在的分子靶点。