Muscarinic cholinergic signaling in cervical cancer cells affects cell motility via ERK1/2 signaling

Parnell, Erinn; Calleja-Macías, Itzel E.; Kalantari, Mina; Grando, Sergei A.; Bernard, Hans‐Ulrich

doi:10.1016/j.lfs.2012.02.020

Cited by 21 publications

(18 citation statements)

References 14 publications

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“…However, the presence of OCT1 and OCT2 in HeLa has not been ascertained. Another still unsolved issue related to the acetylcholine network in HeLa is the mechanism of choline reuptake since ChT choline transporter is not expressed in these cells [13] while choline efflux has been described, associated to expression of SLC44A5 [21]. In the present work, expression and function of OCTN1 in membranes of HeLa cells has been assessed by different experimental approaches.…”

Section: Discussionmentioning

confidence: 93%

“…Very few data are reported about the acetylcholine release mechanisms in cancer cells [20]. This issue was dealt with recently in HeLa cells in which the presence of systems that may mediate acetylcholine transport was analyzed by RT-PCR analysis [13]. A very low if any level of the VAChT mRNA was detected indicating that the corresponding protein is not expressed.…”

Section: Discussionmentioning

confidence: 99%

“…More recently, it was reported that cervical cancer cells express acetylcholine receptors, synthesizing and degrading enzymes, choline acetyltransferase and acetylcholinesterase besides other enzymes involved in acetylcholine metabolism [13]. For paracrine or autocrine signaling, synthesized acetylcholine has to be exported due to the extracellular localization of receptor ligand binding sites [18,25].…”

Section: Introductionmentioning

confidence: 99%

“…Concerning the way of acetylcholine release from these cells, it has been found that SiHa cells contain abundant VAChT mRNA indicating that these cells may express the transporter, while VAChT mRNA is nearly absent in HeLa cells. Moreover ChT, which in nervous tissue catalyzes reuptake of choline, is not expressed in cervical cancer cells [13].…”

Section: Introductionmentioning

confidence: 99%

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Immuno-detection of OCTN1 (SLC22A4) in HeLa cells and characterization of transport function

Pochini

Scalise

Indiveri

2015

International Immunopharmacology

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Immuno-detection of OCTN1 (SLC22A4) in HeLa cells and characterization of transport function

Pochini

Scalise

Indiveri

2015

International Immunopharmacology

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“…Beyond this, acetylcholine receptors may not only affect cervical carcinogenesis after stimulation by tobacco smoking, but polymorphic receptors may even differentially process auto- and paracrine acetylcholine signals and thereby pass thresholds that normally separate tissue homeostasis from neoplastic differentiation processes. Parnell et al (Epub ahead of print) recently demonstrated that cancerous cervical cells express the necessary enzymes for ACh biosynthesis and therefore could participate in autocrine as well as paracrine nAChR activation. The evidence that nAChR antagonists suppress basal migration indicates that the nAChRs are activated, presumably autocrine ACh, without exogenous agonists being added.…”

Section: Discussionmentioning

confidence: 99%

Association of single nucleotide polymorphisms of nicotinic acetylcholine receptor subunits with cervical neoplasia

et al. 2012

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Aims Cholinergic signaling, particularly in response to non-physiological ligands like nicotine, stimulates carcinogenesis of a variety of tissue types including epithelia of the cervix uteri. Cholinergic signaling is mediated by nicotinic acetylcholine receptors (nAChRs), which are pentamers formed by subsets of 16 nAChR subunits. Recent literature suggests that single nucleotide polymorphisms (SNPs) of some of these subunits, notably alpha5, are risk factors for developing lung cancer in smokers as well as in non-smokers. Main methods We have studied the prevalence of four SNPs in the alpha5, alpha9, and beta1 subunits, which are expressed in cervical cells, in 456 patients with cervical cancers, precursor lesions, and healthy controls from two cohorts in Mexico. Key findings A SNP in the alpha9 subunit, the G allele of rs10009228 (alpha9, A>G) shows a significant trend in the combined cohort, indicating that this allele constitutes a risk factor for neoplastic progression. The A allele of the SNP rs16969968 (alpha5, G>A), which correlates with the development of lung cancer, shows a non-significant trend to be associated with cervical lesions. Two other SNPs, rs55633891 (alpha9, C>T) and rs17856697 (beta1, A>G), did not exhibit a significant trend. Significance Our study points to a potential risk factor of cervical carcinogenesis with importance for DNA diagnosis and as a target for intervention.

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MicroRNA‐374b inhibits cervical cancer cell proliferation and induces apoptosis through the p38/ERK signaling pathway by binding to JAM‐2

Cao²,

et al. 2018

Journal Cellular Physiology

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Cervical cancer (CC) remains a highly prevalent cancer and mortality globally among women globally. The aim of the present study was to assess the ability of miR-374b to regulate CC cells through JAM-2, whilst exploring whether the underlying mechanism and its relation to the p38/ERK signaling pathway. During the study, microRNA-374b (miR-374b) was observed to have been expressed at a low level among CC tissues. Hence, a series of miR-374b mimics, miR-374b inhibitors, siRNA against JAM-2, SB202190 (an inhibitor for p38), and PD98059 (an inhibitor for ERK) were introduced to treat CC Siha cells and normal cervical Ect1/E6E7 cells. MTT, flow cytometry, scratch test, and transwell assays were applied to determine cell viability, apoptosis, migration, and invasion. The inhibitory role of the p38/ERK signaling pathway was observed in the CC cells treated with miR-374b mimics or siRNA against JAM-2. miR-374b mimic exposure was found to reduce cell viability, migration, and invasion, but induce apoptosis. MiR-374b inhibitor exposure was observed to have induced effects on the CC cells in a contrary manner to those induced by that of the miR-374b mimics. The key findings of the study demonstrated that miR-374b significantly inhibits cell proliferation, migration, and invasion through the blockade of the p38/ERK signaling pathway activation, as well as negatively binding to JAM-2, highlighting its potential as a therapeutic target for CC.

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Muscarinic cholinergic signaling in cervical cancer cells affects cell motility via ERK1/2 signaling

Cited by 21 publications

References 14 publications

Immuno-detection of OCTN1 (SLC22A4) in HeLa cells and characterization of transport function

Immuno-detection of OCTN1 (SLC22A4) in HeLa cells and characterization of transport function

Association of single nucleotide polymorphisms of nicotinic acetylcholine receptor subunits with cervical neoplasia

MicroRNA‐374b inhibits cervical cancer cell proliferation and induces apoptosis through the p38/ERK signaling pathway by binding to JAM‐2

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