PMID- 33214335
OWN - NLM
STAT- MEDLINE
DCOM- 20210824
LR  - 20210824
IS  - 1899-1505 (Electronic)
IS  - 0867-5910 (Linking)
VI  - 71
IP  - 4
DP  - 2020 Aug
TI  - CD49d and CD49e induce cell adhesion-mediated drug resistance through the nuclear 
      factor-kappaB pathway in Burkitt lymphoma.
LID - 10.26402/jpp.2020.4.02 [doi]
AB  - Burkitt lymphoma (BL) is a highly aggressive form of non-Hodgkin's B-cell 
      lymphoma. Currently, multi-agent chemotherapy regimens are being used to 
      significantly improve cure rates and achieve complete remissions in BL patients. 
      However, drug resistance can often occur within 6 months in BL patients, 
      contributing to poor prognosis. Mounting evidence suggests that cell 
      adhesion-mediated drug resistance (CAM-DR), caused by the interaction between the 
      bone marrow microenvironment and tumour cells may play an important role in drug 
      resistance to chemotherapy. However, the molecular mechanism underlying CAM-DR in 
      BL has not been identified yet. In this study, we investigated the molecular 
      mechanism responsible for CAM-DR in BL cells. We also examined the therapeutic 
      targets of CAM-DR in BL cells and found CD49d and CD49e to be the important 
      adhesion molecules involved. However, CD49a, CD49b, CD11a, CD29, CD18, and CD61 
      were not found to be associated with CAM-DR in BL cells. Furthermore, we 
      clarified that CD49d- and CD49e-mediated CAM-DR could be attributed to an 
      increase in the expression of B cell leukemia-xL (Bcl-xL) and survivin proteins, 
      and a decrease in the expression of Bcl-2 associated X (Bax), Bcl-2 interacting 
      mediator (Bim) and p53 upregulated modulator of apoptosis (PUMA) proteins via 
      nuclear factor kappaB (NF-kappaB) activation. In addition, bortezomib was found to 
      overcome CAM-DR in BL cells by inhibiting NF-kappaB. Thus, bortezomib may have 
      potential clinical applications in the treatment of CD49d- and CD49e-mediated 
      CAM-DR in BL patients.
FAU - Takeda, T
AU  - Takeda T
AD  - Division of Pharmacotherapy, Kindai University School of Pharmacy, Kowakae, 
      Higashi-Osaka, Osaka, Japan.
FAU - Tsubak, M
AU  - Tsubak M
AD  - Division of Pharmacotherapy, Kindai University School of Pharmacy, Kowakae, 
      Higashi-Osaka, Osaka, Japan.
FAU - Genno, S
AU  - Genno S
AD  - Division of Pharmacotherapy, Kindai University School of Pharmacy, Kowakae, 
      Higashi-Osaka, Osaka, Japan.
FAU - Matsuda, T
AU  - Matsuda T
AD  - Division of Pharmacotherapy, Kindai University School of Pharmacy, Kowakae, 
      Higashi-Osaka, Osaka, Japan.
FAU - Yamamoto, Y
AU  - Yamamoto Y
AD  - Division of Pharmacotherapy, Kindai University School of Pharmacy, Kowakae, 
      Higashi-Osaka, Osaka, Japan.
FAU - Ueda, E
AU  - Ueda E
AD  - Division of Pharmacotherapy, Kindai University School of Pharmacy, Kowakae, 
      Higashi-Osaka, Osaka, Japan.
FAU - Imano, M
AU  - Imano M
AD  - Department of Surgery, Kindai University School of Medicine, Osakasayama, Osaka, 
      Japan.
FAU - Satou, T
AU  - Satou T
AD  - Department of Pathology, Kindai University School of Medicine, Osakasayama, 
      Osaka, Japan.
FAU - Nishida, S
AU  - Nishida S
AD  - Division of Pharmacotherapy, Kindai University School of Pharmacy, Kowakae, 
      Higashi-Osaka, Osaka, Japan. nishida@phar.kindai.ac.jp.
LA  - eng
PT  - Journal Article
DEP - 20201115
PL  - Poland
TA  - J Physiol Pharmacol
JT  - Journal of physiology and pharmacology : an official journal of the Polish 
      Physiological Society
JID - 9114501
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Apoptosis Regulatory Proteins)
RN  - 0 (Integrin alpha5)
RN  - 0 (NF-kappa B)
RN  - 0 (Proteasome Inhibitors)
RN  - 143198-26-9 (Integrin alpha4)
RN  - 69G8BD63PP (Bortezomib)
SB  - IM
MH  - Animals
MH  - Antineoplastic Agents/*pharmacology
MH  - Apoptosis Regulatory Proteins/metabolism
MH  - Bortezomib/pharmacology
MH  - Burkitt Lymphoma/*drug therapy/immunology/metabolism
MH  - Cell Adhesion/*drug effects
MH  - Cell Line, Tumor
MH  - Coculture Techniques
MH  - *Drug Resistance, Neoplasm
MH  - Humans
MH  - Integrin alpha4/*metabolism
MH  - Integrin alpha5/*metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - NF-kappa B/*metabolism
MH  - Proteasome Inhibitors/pharmacology
MH  - Signal Transduction
MH  - Tumor Microenvironment
EDAT- 2020/11/21 06:00
MHDA- 2021/08/25 06:00
CRDT- 2020/11/20 05:43
PHST- 2020/06/11 00:00 [received]
PHST- 2020/08/29 00:00 [accepted]
PHST- 2020/11/20 05:43 [entrez]
PHST- 2020/11/21 06:00 [pubmed]
PHST- 2021/08/25 06:00 [medline]
AID - 10.26402/jpp.2020.4.02 [doi]
PST - ppublish
SO  - J Physiol Pharmacol. 2020 Aug;71(4). doi: 10.26402/jpp.2020.4.02. Epub 2020 Nov 
      15.