PMID- 37323178
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230619
IS  - 2218-6751 (Print)
IS  - 2226-4477 (Electronic)
IS  - 2218-6751 (Linking)
VI  - 12
IP  - 5
DP  - 2023 May 31
TI  - Inhibition of BPHL inhibits proliferation in lung carcinoma cell lines.
PG  - 1051-1061
LID - 10.21037/tlcr-23-225 [doi]
AB  - BACKGROUND: Lung cancer is one of the most common human malignant tumors and the 
      leading cause of cancer death worldwide. Biphenyl hydrolase-like (BPHL) is a gene 
      encoding the human BPHL enzyme, a serine hydrolase that catalyzes the hydrolytic 
      activation of amino acid ester prodrugs of nucleoside analogs such as 
      valacyclovir and valganciclovir. However, the role of BPHL in lung cancer is 
      still unknown. METHODS: In this study, we assessed the effect BPHL knockdown on 
      the proliferation, apoptosis, colony formation, metastasis, and cell cycle of 
      cancer cells. BPHL knockdown NCI-H1299 and A549 cells demonstrated decreased 
      proliferation, as measured by Celigo cell counting. The MTT assay results were 
      consistent with Celigo cell counting. Caspase 3/7 activity increased 
      significantly in the NCI-H1299 and A549 cells after shBPHL knockdown. Decreased 
      colony formation in the NCI-H1299 and A54 cells after shBPHL knockdown, as 
      measured by crystal violet staining. Transmigration assay using a Transwell 
      demonstrated that there were significantly fewer migrating cells in the lower 
      chamber in the BPHL knockdown NCI-H1299 and A549 cells. Cell cycle analysis by 
      Propidium Iodide (PI) staining and fluorescence activated cell sorter (FACS). We 
      also explored the effect of BPHL knockdown on tumor growth in a mouse model of 
      tumor implantation in nude mice. RESULTS: We found that the knockdown of BPHL 
      gene expression by short hairpin RNA (shRNA) leads to a decrease in 
      proliferation, colony formation, and metastasis and an increase in apoptosis in 
      two lung adenocarcinoma (LUAD) cell lines in vitro. BPHL knockdown induces 
      decreased tumor growth, colony formation, and metastasis; increased apoptosis; 
      and altered cell cycle destruction. BPHL knockdown results in decreased tumor 
      growth in vivo. Moreover, BPHL knockdown A549 cells demonstrated slower growth 
      compared to control cells upon implantation in nude mice, confirming the in vitro 
      findings. CONCLUSIONS: In this study, the data indicate that BPHL potentially 
      promotes proliferation, inhibits apoptosis, and increases colony formation and 
      metastasis in lung cancer. Overall, our study suggests that BPHL may be a gene 
      that promotes tumor growth in lung cancer.
CI  - 2023 Translational Lung Cancer Research. All rights reserved.
FAU - Ren, Pengfei
AU  - Ren P
AD  - Department of Thoracic Surgery, Nanfang Hospital, Southern Medical University, 
      Guangzhou, China.
FAU - Zhai, Jianxue
AU  - Zhai J
AD  - Department of Thoracic Surgery, Nanfang Hospital, Southern Medical University, 
      Guangzhou, China.
FAU - Wang, Xuelian
AU  - Wang X
AD  - Department of Anesthesiology (Operating Room), The Third Affiliated Hospital of 
      Southern Medical University, Guangzhou, China.
FAU - Yin, Yucheng
AU  - Yin Y
AD  - Department of Thoracic Surgery, Nanfang Hospital, Southern Medical University, 
      Guangzhou, China.
FAU - Lin, Zuju
AU  - Lin Z
AD  - Department of Thoracic Surgery, Nanfang Hospital, Southern Medical University, 
      Guangzhou, China.
FAU - Cai, Kaican
AU  - Cai K
AD  - Department of Thoracic Surgery, Nanfang Hospital, Southern Medical University, 
      Guangzhou, China.
FAU - Wang, Haofei
AU  - Wang H
AD  - Department of Thoracic Surgery, Nanfang Hospital, Southern Medical University, 
      Guangzhou, China.
LA  - eng
PT  - Journal Article
DEP - 20230529
PL  - China
TA  - Transl Lung Cancer Res
JT  - Translational lung cancer research
JID - 101646875
PMC - PMC10261862
OTO - NOTNLM
OT  - Biphenyl hydrolase-like (BPHL)
OT  - inhibits proliferation
OT  - lung carcinoma cell lines
COIS- Conflicts of Interest: All authors have completed the ICMJE uniform disclosure 
      form (available at 
      https://tlcr.amegroups.com/article/view/10.21037/tlcr-23-225/coif). The authors 
      have no conflicts of interest to declare.
EDAT- 2023/06/16 06:42
MHDA- 2023/06/16 06:43
PMCR- 2023/05/31
CRDT- 2023/06/16 03:55
PHST- 2023/03/03 00:00 [received]
PHST- 2023/05/16 00:00 [accepted]
PHST- 2023/05/29 00:00 [accepted]
PHST- 2023/06/16 06:43 [medline]
PHST- 2023/06/16 06:42 [pubmed]
PHST- 2023/06/16 03:55 [entrez]
PHST- 2023/05/31 00:00 [pmc-release]
AID - tlcr-12-05-1051 [pii]
AID - 10.21037/tlcr-23-225 [doi]
PST - ppublish
SO  - Transl Lung Cancer Res. 2023 May 31;12(5):1051-1061. doi: 10.21037/tlcr-23-225. 
      Epub 2023 May 29.