SMEK1 promotes lung adenocarcinoma proliferation and invasion by activating Wnt/β-catenin signaling pathway

Chen, Dandan; Gao, Shang; Gao, Fei; Liu, Ai; Li, Jiangxia; Li, Jisheng; Liu, Qiji

doi:10.1007/s12094-022-03001-8

Cited by 4 publications

(3 citation statements)

References 43 publications

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“…β-Catenin protein expression is also upregulated by FOXH1 [ 123 ], LRP8 [ 124 ], CBX4 [ 125 ], SMEK1 [ 126 ], JAML [ 127 ], ERCC6L [ 128 ], NOVA1 [ 129 ], SETDB1 [ 130 ], HMGB1 [ 131 ] and DEPDC1B [ 132 ] (Table 2 ), though the underlying molecular mechanism remains elusive. Additional regulators specifically mediate the level of active (i.e., unphosphorylated at Ser33/Ser37/Thr41) β‐catenin.…”

Section: The Positive Regulators Of Wnt/β-catenin Signalingmentioning

confidence: 99%

Wnt/β-catenin signaling in the development and therapeutic resistance of non-small cell lung cancer

Zhang,

Westover,

Tang

et al. 2024

J Transl Med

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Wnt/β-catenin signaling is a critical pathway that influences development and therapeutic response of non-small cell lung cancer (NSCLC). In recent years, many Wnt regulators, including proteins, miRNAs, lncRNAs, and circRNAs, have been found to promote or inhibit signaling by acting on Wnt proteins, receptors, signal transducers and transcriptional effectors. The identification of these regulators and their underlying molecular mechanisms provides important implications for how to target this pathway therapeutically. In this review, we summarize recent studies of Wnt regulators in the development and therapeutic response of NSCLC.

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Section: The Positive Regulators Of Wnt/β-catenin Signalingmentioning

confidence: 99%

Wnt/β-catenin signaling in the development and therapeutic resistance of non-small cell lung cancer

Zhang,

Westover,

Tang

et al. 2024

J Transl Med

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“…Subsequent follow-up assessments were conducted for these PTC patients. Notably, the average age of diagnosis for these individuals was at 28.5 (19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33) years. During the follow-up period, patient III 5, diagnosed with thyroid cancer at the age of 19, experienced a recurrence and lymph node metastasis, confirmed through aspiration, and subsequently underwent a re-operative surgery.…”

Section: Clinical Characteristics Of the Nmtc Familymentioning

confidence: 99%

“…It has been shown to exert anti-angiogenic effects in ovarian tumors by inhibiting the VEGFR-2-mediated PI3K/Akt/eNOS signaling pathway [31] and interacting with the tumor suppressor BLU, resulting in pro-apoptotic activity in cervical and ovarian cancers [32]. Conversely, a recent study suggested that PPP4R3A promotes carcinogenesis in lung adenocarcinoma by activating the Wnt/β-catenin signaling pathway [33].…”

Section: Introductionmentioning

confidence: 99%

Identification of a Novel Germline PPP4R3A Missense Mutation Asp409Asn on Familial Non-Medullary Thyroid Carcinoma

Hu,

Han,

Guo

et al. 2024

Biomedicines

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Familial non-medullary thyroid carcinoma (FNMTC) accounts for 3% to 9% of all thyroid cancer cases, yet its genetic mechanisms remain unknown. Our study aimed to screen and identify novel susceptibility genes for FNMTC. Whole-exome sequencing (WES) was conducted on a confirmed FNMTC pedigree, comprising four affected individuals across two generations. Variants were filtered and analyzed using ExAC and 1000 Genomes Project, with candidate gene pathogenicity predicted using SIFT, PolyPhen, and MutationTaster. Validation was performed through Sanger sequencing in affected pedigree members and sporadic patients (TCGA database) as well as general population data (gnomAD database). Ultimately, we identified the mutant PPP4R3A (NC_000014.8:g.91942196C>T, or NM_001366432.2(NP_001353361.1):p.(Asp409Asn), based on GRCH37) as an FNMTC susceptibility gene. Subsequently, a series of functional experiments were conducted to investigate the impact of PPP4R3A and its Asp409Asn missense variant in thyroid cancer. Our findings demonstrated that wild-type PPP4R3A exerted tumor-suppressive effects via the Akt-mTOR-P70 S6K/4E-BP1 axis. However, overexpression of the PPP4R3A Asp409Asn mutant resulted in loss of tumor-suppressive function, ineffective inhibition of cell invasion, and even promotion of cell proliferation and migration by activating the Akt/mTOR signaling pathway. These results indicated that the missense variant PPP4R3A Asp409Asn is a candidate susceptibility gene for FNMTC, providing new insights into the diagnosis and intervention of FNMTC.

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SMEK1 promotes clear cell Renal Cell Carcinoma progression via EGFR tyrosine-kinase dependent pathway

Wang,

Bi,

et al. 2024

Cancer Letters

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SMEK1 promotes lung adenocarcinoma proliferation and invasion by activating Wnt/β-catenin signaling pathway

Cited by 4 publications

References 43 publications

Wnt/β-catenin signaling in the development and therapeutic resistance of non-small cell lung cancer

Wnt/β-catenin signaling in the development and therapeutic resistance of non-small cell lung cancer

Identification of a Novel Germline PPP4R3A Missense Mutation Asp409Asn on Familial Non-Medullary Thyroid Carcinoma

SMEK1 promotes clear cell Renal Cell Carcinoma progression via EGFR tyrosine-kinase dependent pathway

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