L1CAM: Cell adhesion and more

Samatov, Timur R.; Wicklein, Daniel; Tonevitsky, Alexander G.

doi:10.1016/j.proghi.2016.05.001

Cited by 69 publications

(59 citation statements)

References 95 publications

(103 reference statements)

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“…Although the role of neural cell adhesion molecules has been widely described to contribute to cancer pathogenesis17, 18, 19, 20, 21, 22, 23 and nonparaneoplastic autoimmune neuropathies,10, 24, 25 the results in our study suggest that nerve damage in our cohort cannot be attributed to a humoral autoimmune attack targeting L1CAM and NCAM1 or the nodal/paranodal CNTN1/CASPR1 complex, CNTN1, NF140, NF155, or NF186. However, this lack of antibodies should be confirmed in further studies involving other cohorts of PN.…”

Section: Discussioncontrasting

confidence: 53%

“…Two of our CIDP patients harboring antibodies against CNTN1, respectively, developed a lymphoma and a colon adenocarcinoma in addition to their neuropathy, one of them concomitantly, and the other several years later. The role of other cell adhesion molecules such as neural cell adhesion molecule 1 (NCAM1)17, 18, 19, 20 and L1 (L1CAM)21, 22, 23 in cancer pathogenesis has been widely described. However, their possible involvement as antigens in paraneoplastic neuropathies has not been studied.…”

Section: Introductionmentioning

confidence: 99%

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Antibodies against cell adhesion molecules and neural structures in paraneoplastic neuropathies

Siles

Martínez‐Hernández

Araque

et al. 2018

Ann Clin Transl Neurol

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ObjectiveParaneoplastic neurological syndromes (PNS) are rare neurological disorders in which ectopic expression of neural antigens by a tumor results in an autoimmune attack against the nervous system. Onconeural antibodies not only guide PNS diagnosis but may also help detecting underlying malignancies. Our project aims to uncover new potential antibodies in paraneoplastic neuropathies (PN).MethodsThirty‐four patients fulfilling diagnostic criteria of possible (n = 9; 26.5%) and definite (n = 25; 73.5%) PN without onconeural antibodies and 28 healthy controls were included in our study. Sera were tested for known antibodies against neural cell adhesion molecules and screened for novel IgG and IgM reactivities against nerve components: dorsal root ganglia (DRG) neurons, motor neurons, and Schwann cells. Patients showing autoantibodies against any of these cell types were used for immunoprecipitation (IP) studies.ResultsOverall, 9 (26.5%) patients showed significant reactivity against DRG neurons, motor neurons, or Schwann cells, whereas 5 (17.9%) healthy controls only showed moderate reactivity. Compared with control sera, serum samples from patients with paraneoplastic sensory‐motor neuropathies had a higher frequency of IgM antibodies against Schwann cells (0% vs. 40%; P = 0.0028). No novel antigens were identified from our IP experiments. Antibodies against the neural adhesion molecules CNTN1, NF155, NF140, NF186, NCAM1, L1CAM, and the CNTN1/CASPR1 complex were not detected in patients with PN. One (2.9%) patient with CIDP and thymoma had CASPR2 antibodies.InterpretationAlmost 30% of patients with PN harbor antibodies targeting neural structures, suggesting that novel neoplasm‐associated antigens remain to be discovered.

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Section: Discussioncontrasting

confidence: 53%

Section: Introductionmentioning

confidence: 99%

Antibodies against cell adhesion molecules and neural structures in paraneoplastic neuropathies

Siles

Martínez‐Hernández

Araque

et al. 2018

Ann Clin Transl Neurol

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“…The prognostic relevance of L1CAM has been demonstrated in several different cancers, with L1CAM shown to be a promising target for anti-cancer therapy (Altevogt et al, 2016; Samatov et al, 2016). However, its functional role in cells with activating KRAS mutation has not yet been clearly shown.…”

Section: Discussionmentioning

confidence: 99%

“…L1CAM was originally identified as a neural cell adhesion molecule that plays an essential role in the development of the nervous system (Grumet and Edelman, 1988). Subsequently, L1CAM has been found to be aberrantly expressed in a variety of malignant tumors, including ovarian cancer, melanoma, breast cancer, gastric cancer, colorectal cancer, non-small cell lung cancer, pancreatic cancer, neuroblastoma, and cholangiocarcinoma, and its expression correlates with a poor prognosis and metastasis (Altevogt et al, 2016; Chen et al, 2013; Jung et al, 2011; Li et al, 2009; Min et al, 2010; Samatov et al, 2016; Weidle et al, 2009). Studies on the cellular functions of L1CAM have demonstrated its promotion of cellular proliferation, migration, invasion, and chemoresistance (Kiefel et al, 2012; Raveh et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

L1 Cell Adhesion Molecule Promotes Migration and Invasion via JNK Activation in Extrahepatic Cholangiocarcinoma Cells with Activating KRAS Mutation

Kim

Hwang

Lee

et al. 2017

Molecules and Cells

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Extrahepatic cholangiocarcinoma (ECC), a malignant tumor of biliary origin, has a poor prognosis with limited treatment options. The KRAS oncogene is the most commonly mutated gene in ECC and one of the factors that predicts a poor prognosis and low survival rate. L1 cell adhesion molecule (L1CAM) is expressed in ECC cells and acts as an independent poor prognostic factor in predicting patient survival. In this study we investigate the functional significance of L1CAM in ECC cells with activating KRAS mutation. We selected an ECC cell line, EGI-1, with activating KRAS mutation, and then confirmed its expression of L1CAM by RT-PCR, western blot analysis, and flow cytometry. The suppression of L1CAM expression (using a specific lentivirus-delivered shRNA) significantly decreased the migratory and invasive properties of EGI-1 cells, without altering their proliferation or survival. Analyses of signaling effectors in L1CAM-depleted and control EGI-1 cells indicated that L1CAM suppression decreased the levels of both phosphorylated MKK4 and total MKK4, together with c-Jun N-terminal kinase (JNK) phosphorylation. Further, exposure to a JNK inhibitor (SP600125) decreased migration and invasion of EGI-1 cells. These results suggest that L1CAM promotes cellular migration and invasion via the induction of MKK4 expression, leading to JNK activation. Our study is the first to demonstrate a functional role for L1CAM in ECC carrying the activating KRAS mutation. Given that KRAS is the most commonly mutated oncogene in ECC, L1CAM may serve as an attractive therapeutic target for ECC cells with activating KRAS mutation.

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“…The L1 cell adhesion molecule (L1CAM; CD171) is a 200–220 kDa membrane glycoprotein that is thought to be involved in the pathogenesis of cancers by increasing their motility, invasiveness, growth and transformation rate . Expression of L1CAM has been found to be a negative prognostic factor in numerous cancers, and therapies that target the L1CAM protein is a subject of ongoing investigations .…”

Section: Clinicopathological Features Of Data Set Including Stratifimentioning

confidence: 99%

The significance of L1CAM expression in clear cell carcinoma of the endometrium

et al. 2017

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L1CAM: Cell adhesion and more

Cited by 69 publications

References 95 publications

Antibodies against cell adhesion molecules and neural structures in paraneoplastic neuropathies

Antibodies against cell adhesion molecules and neural structures in paraneoplastic neuropathies

L1 Cell Adhesion Molecule Promotes Migration and Invasion via JNK Activation in Extrahepatic Cholangiocarcinoma Cells with Activating KRAS Mutation

The significance of L1CAM expression in clear cell carcinoma of the endometrium

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