2. Academic Validation
  3. Aberrant expression of GOLM1 protects ALK+ anaplastic large cell lymphoma from apoptosis by enhancing BCL-XL stability

Aberrant expression of GOLM1 protects ALK+ anaplastic large cell lymphoma from apoptosis by enhancing BCL-XL stability

  • Blood Adv. 2023 Feb 10;bloodadvances.2022008384. doi: 10.1182/bloodadvances.2022008384.
Zhenguo Zi 1,  Shujuan Du 2,  Liming Zhang 3,  Yuebo Wang 1,  Ling Ding 4,  Chongqi Zhang 1,  Huanyu Wang 1,  Jan Pawlicki 5,  Yuan Cai 6,  Yazhou Yao 7,  Feng Zhou 2,  Yin Tong 8,  James L Riley 9,  Qiliang Cai 10,  Xiaojing Ma 11,  Fang Wei 1
Affiliations

Affiliations

  • 1 Shanghai Jiao Tong University, Shanghai, China.
  • 2 Fudan University, Shanghai, China.
  • 3 Jiangxi Cancer Hospital, Nanchang, China.
  • 4 Fudan University.
  • 5 University of Pennsylvania, Philadelphia, Pennsylvania, United States.
  • 6 Department of Pathology, Baoji Central Hospital, Baoji, China.
  • 7 Department of Hematology, Baoji, China.
  • 8 Shanghai Jiao-Tong University School of Medicine.
  • 9 University of Pennsylvania, Perelman School of Medicine, Philadelphia, Pennsylvania, United States.
  • 10 Fudan University School of Basic Medical Science, Shanghai, China.
  • 11 Weill Medical College of Cornell University, New York, New York, United States.
PMID: 36763539 DOI: 10.1182/bloodadvances.2022008384
Abstract

Golgi membrane protein 1 (GOLM1) is aberrantly expressed in many types of solid tumors and contributes to Cancer development; however, its role in hematopoietic and lymphoid neoplasms remains unknown. Here, we report that GOLM1 was significantly upregulated in anaplastic large cell lymphoma (ALCL), particularly in anaplastic lymphoma kinase-positive (ALK+) ALCL. Mechanistically, the expression of GOLM1 was induced by nucleophosmin (NPM)-ALK in both ALK-transformed T cells and ALCL cell lines through Akt/mTOR pathway. Knockdown of GOLM1 expression led to a reduction in the growth and viability of ALCL cells with increased spontaneous Apoptosis, while ectopic expression of GOLM1 protected ALCL cells from Apoptosis induced by staurosporine treatment. Moreover, GOLM1 directly interacted with B-cell lymphoma-extra-large protein (Bcl-xL, a crucial anti-apoptosis regulator) and significantly prolonged its stability. Introduction of GOLM1 promoted ALK+ ALCL cells colony formation in vitro and tumor growth in a murine xenograft model. Taken together, our findings demonstrate for the first time that GOLM1 plays a critical role in suppressing Apoptosis and promoting the progression of ALK+ ALCL and provide evidence that GOLM1 is a potential biomarker and therapeutic target in ALK-induced hematological malignancies.

Figures
Products
嗨！很高兴为您提供帮助！

尊敬的 MCE 客户您好，
请您选择所在区域，我们将转接对应客服为您服务！

热门区域

A

B

C

F

G

H

J

L

N

Q

S

T

X

Y

Z

热 A B C F G H J L N Q S T X Y Z