Wang Yin, Hu Xiaoli, Song Yaqi, Ruan Qianqi, Bai Xiaoteng, Du Juan
Department of Hematology, Myeloma & Lymphoma Center, Shanghai Changzheng Hospital, Shanghai, 200003, China.
The First Clinical Medical College, Lanzhou University, Lanzhou, 730099, China.
Mol Biol Rep. 2025 Jul 1;52(1):664. doi: 10.1007/s11033-025-10749-z.
Calreticulin (CALR) has been implicated in the genesis and progression of numerous tumors. Nevertheless, its impact on multiple myeloma (MM) remains ambiguous. This study aimed to explore the effect of CALR on the proliferation and drug sensitivity of MM cells and to delve into its underlying mechanism.
First, the expression of CALR in MM cells was measured. Subsequently, the impact of CALR knockdown on MM cells was validated both in vitro and in vivo. Finally, RNA sequencing was utilized to explore the molecular mechanisms associated with CALR knockdown.
We determined that CALR is upregulated in myeloma cells. Both in vitro and in vivo functional assays demonstrated that CALR knockdown attenuated the proliferative capacity of MM cells, heightened their sensitivity to bortezomib (BTZ), and facilitated MM cell apoptosis. RNA-sequencing results indicated that CALR knockdown activates the apoptosis pathway, with the underlying mechanism potentially involving the regulation of the BCL2 signaling pathway.
This study indicates that CALR is associated with the proliferation and drug sensitivity of MM. Targeting CALR might be a potential strategy to further enhance the treatment efficacy for MM.
Not applicable.
钙网蛋白（CALR）与多种肿瘤的发生和进展有关。然而，其对多发性骨髓瘤（MM）的影响仍不明确。本研究旨在探讨CALR对MM细胞增殖和药物敏感性的影响，并深入研究其潜在机制。
首先，检测MM细胞中CALR的表达。随后，在体外和体内验证CALR敲低对MM细胞的影响。最后，利用RNA测序探索与CALR敲低相关的分子机制。
我们确定CALR在骨髓瘤细胞中上调。体外和体内功能试验均表明，CALR敲低减弱了MM细胞的增殖能力，提高了其对硼替佐米（BTZ）的敏感性，并促进了MM细胞凋亡。RNA测序结果表明，CALR敲低激活了凋亡途径，其潜在机制可能涉及对BCL2信号通路的调节。
本研究表明CALR与MM的增殖和药物敏感性相关。靶向CALR可能是进一步提高MM治疗疗效的潜在策略。
不适用。
