PMID- 38545258
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240329
IS  - 1873-9601 (Print)
IS  - 1873-961X (Electronic)
IS  - 1873-9601 (Linking)
VI  - 18
IP  - 1
DP  - 2024 Mar
TI  - IncRNA AC004943.2 regulates miR-135a-5p and PTK2/P13K axis to promote laryngeal 
      squamous cell carcinoma progression.
PG  - e12016
LID - 10.1002/ccs3.12016 [doi]
LID - e12016
AB  - Long noncoding RNAs (lncRNAs) are involved in regulatory processes in laryngeal 
      squamous cell carcinoma (LSCC) at posttranscriptional epigenetic modification 
      level. Yet, the function and underlying mechanism behind lncRNA AC004943.2 in 
      LSCC is still obscure. Therefore, the potential role of AC004943.2 in LSCC 
      progression was investigated. The expression of gene or protein was tested by 
      real-time quantitative polymerase chain reaction and western blot. MTT, colony 
      formation, wound healing, and transwell experiments were applied to detect LSCC 
      cell viability, proliferation, migration and invasion, respectively. The 
      interaction among AC004943.2, miR-135a-5p, and protein tyrosine kinase 2 (PTK2) 
      were analyzed by bioinformatics prediction and luciferase assay. AC004943.2 was 
      highly expressed in LSCC cells compared with normal human bronchial epithelial 
      cells, while miR-135a-5p was lowly expressed. AC004943.2 knockdown or miR-135a-5p 
      overexpression inhibited LSCC cell viability, proliferation, migration and 
      invasion. Mechanistically, AC004943.2 increased PTK2 expression in LSCC cells by 
      sponging miR-135a-5p. Furthermore, miR-135a-5p knockdown inverted the inhibitory 
      effect of AC004943.2 silencing on LSCC cell malignant behaviors. MiR-135a-5p 
      upregulation attenuated the PTK2/PI3K pathway to inhibit progression of LSCC. 
      AC004943.2 facilitated the cancerous phenotypes of LSCC cells by activating the 
      PTK2/PI3K pathway through targeting miR-135a-5p, which furnished a therapeutic 
      candidate for LSCC treatment.
CI  - (c) 2024 The Authors. Journal of Cell Communication and Signaling published by John 
      Wiley & Sons Ltd.
FAU - Zhu, Xiaowen
AU  - Zhu X
AD  - Department of General Surgery Fourth Ward The First Affiliated Hospital of 
      Jiamusi University Jiamusi Heilongjiang Province China.
FAU - Dong, Wenming
AU  - Dong W
AD  - Department of Anesthesiology Shenzhen Baoan Hospital of TCM Shenzhen Guangdong 
      Province China.
FAU - Zhang, Meijia
AU  - Zhang M
AUID- ORCID: 0009-0003-8857-3822
AD  - Department of Otolaryngology The First Affiliated Hospital of Jiamusi University 
      Jiamusi Heilongjiang Province China.
LA  - eng
PT  - Journal Article
DEP - 20240209
PL  - United States
TA  - J Cell Commun Signal
JT  - Journal of cell communication and signaling
JID - 101308338
PMC - PMC10964940
OTO - NOTNLM
OT  - AC004943.2
OT  - PI3K
OT  - PTK2
OT  - laryngeal squamous cell carcinoma
OT  - miR-135a-5p
COIS- The authors declare that they have no conflict of interest.
EDAT- 2024/03/28 06:44
MHDA- 2024/03/28 06:45
PMCR- 2024/02/09
CRDT- 2024/03/28 04:07
PHST- 2023/10/11 00:00 [received]
PHST- 2023/12/29 00:00 [revised]
PHST- 2023/12/29 00:00 [accepted]
PHST- 2024/03/28 06:45 [medline]
PHST- 2024/03/28 06:44 [pubmed]
PHST- 2024/03/28 04:07 [entrez]
PHST- 2024/02/09 00:00 [pmc-release]
AID - CCS312016 [pii]
AID - 10.1002/ccs3.12016 [doi]
PST - epublish
SO  - J Cell Commun Signal. 2024 Feb 9;18(1):e12016. doi: 10.1002/ccs3.12016. 
      eCollection 2024 Mar.