ERK signaling for cell migration and invasion

Samson, Shiela C.; Khan, Akib M.; Mendoza, Michelle C.

doi:10.3389/fmolb.2022.998475

Cited by 46 publications

(31 citation statements)

References 91 publications

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“…The result indicated that the cell migration got markedly reduced after targeted inhibition by siRNA showing that ERK may have a role on cell adhesion molecules. This is in accordance with many recent evidences (Hunter et al, 2022).Evidences from the cell invasion assay also indicated that specific ERK modulation can actually change cell invasion rate suggesting an ERK dependent ECM theory (Samson et al, 2022).…”

Section: Table 3: Values Of Parameters With Control Group With Respec...supporting

confidence: 92%

Studies of Erk1/2 with Respect to Tumor Aggressiveness in B16f10 Murine Melanoma Cells

-¹,

-²,

-³

et al. 2023

IJFMR

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Melanoma is a very aggressive form of skin cancer and have the potential to spread from a small sized primary tumor and metastasizes to different locations like lungs, bones, lymph nodes, liver and even brain. Extracellular signal regulated kinase (ERK) molecule present in MAPK pathway plays a major role in different carcinogenic processes like cell migration, cell invasiveness by altering the extracellular matrix (ECM). Cell invasiveness is facilitated by matrix metalloproteins (MMPs) by means of degradation of gelatinase enzyme regulated by a family of receptor proteins called integrins. ECM ligand fibronectin causes increased secretion of MMPs, specially MMP2 and MMP9 facilitating invasiveness and metastasis in cancer cells. This study aims to find the modulatory role of ERK 1/ 2 with respect to tumor aggressiveness on both MMP2 and MMP9 on melanoma metastasis and invasion. ERK pathway was downregulated through administration of inhibitors and ERK 1/ 2 siRNA gene silencing the effect on MMP2 and MMP9 was studied. The studies were done in B16F10 melanoma cell line and mice model. Significant changes were found in levels of MMP2 and MMP9 after downregulating the ERK pathway and can therefore a correlation between ERK and MMP activities was concluded. Elucidating these molecular phenomena in melanoma, this result can help in developing and improving targeted cancer therapies with multiple options in drug discovery.

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Section: Table 3: Values Of Parameters With Control Group With Respec...supporting

confidence: 92%

Studies of Erk1/2 with Respect to Tumor Aggressiveness in B16f10 Murine Melanoma Cells

-¹,

-²,

-³

et al. 2023

IJFMR

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“…We also showed that ORF21 mediated the upregulation of the MEK pathway and anchorage-independent cell growth ( Figure 7 ). Although RhoA–ROCK signaling is well known to promote cell migration [ 32 , 33 ], the MEK pathway has also been reported to contribute to the promotion of cell migration [ 34 , 35 , 36 , 37 ].…”

Section: Discussionmentioning

confidence: 99%

Kaposi’s Sarcoma-Associated Herpesvirus ORF21 Enhances the Phosphorylation of MEK and the Infectivity of Progeny Virus

Yamaguchi

Watanabe

Iwaisako

et al. 2023

IJMS

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Kaposi’s sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus-8, is the causative agent of Kaposi’s sarcoma, Castleman’s disease, and primary effusion lymphoma. Although the functions of the viral thymidine kinases (vTK) of herpes simplex virus-1/2 are well understood, that of KSHV ORF21 (an ortholog of vTK) is largely unknown. Here, we investigated the role of ORF21 in lytic replication and infection by generating two ORF21-mutated KSHV BAC clones: ORF21-kinase activity deficient KSHV (21KD) and stop codon-induced ORF21-deleted KSHV (21del). The results showed that both ORF21 mutations did not affect viral genome replication, lytic gene transcription, or the production of viral genome-encapsidated particles. The ORF21 molecule-dependent function, other than the kinase function of ORF21, was involved in the infectivity of the progeny virus. ORF21 was expressed 36 h after the induction of lytic replication, and endogenously expressed ORF21 was localized in the whole cytoplasm. Moreover, ORF21 upregulated the MEK phosphorylation and anchorage-independent cell growth. The inhibition of MEK signaling by U0126 in recipient target cells suppressed the number of progeny virus-infected cells. These suggest that ORF21 transmitted as a tegument protein in the progeny virus enhances the new infection through MEK up-regulation in the recipient cell. Our findings indicate that ORF21 plays key roles in the infection of KSHV through the manipulation of the cellular function.

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“…7). Although RhoA-ROCK signaling is well known to promote cell migration [32,33], the MEK pathway has also been reported to contribute to the promotion of cell migration [34][35][36][37].…”

Section: Discussionmentioning

confidence: 99%

Kaposi’s Sarcoma-associated Herpesvirus ORF21 Enhances the Phosphorylation of MEK and the Infectivity of Progeny Virus

Yamaguchi¹,

Watanabe²,

Iwaisako³

et al. 2022

Preprint

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Kaposi’s sarcoma-associated herpesvirus (KSHV), also known as human herpesvirus-8, is the causative agent of Kaposi’s sarcoma, Castleman’s disease, and primary effusion lymphoma. Although the functions of the viral thymidine kinases (vTK) of herpes simplex virus-1/2 and varicella zoster virus are well understood, that of KSHV ORF21 (an ortholog of vTK) is largely unknown. Here, we investigated the role of ORF21 in lytic replication and infection by generating two ORF21-mutated KSHV BAC clones: ORF21-kinase activity deficient-KSHV (21KD) and stop codon-induced ORF21-deleted-KSHV (21del). The results showed that both ORF21-mutations did not affect viral genome replication, lytic genes transcription, or the production of viral genome-encapsidated particles. ORF21 molecule-dependent function, other than the kinase function of ORF21, was involved in the infectivity of progeny virus. ORF21 was expressed at 36 h after induction of lytic replication, and endogenously expressed ORF21 was localized in the whole cytoplasm and decreased on the cell surface area. Moreover, the effects of ORF21 expression on signaling pathways and proliferation were analyzed. The results showed that ORF21 upregulated the MEK phosphorylation and anchorage-independent cell growth. These findings indicate that ORF21 plays key roles in both infection and oncogenesis of KSHV through the manipulation of cellular function.

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ERK signaling for cell migration and invasion

Cited by 46 publications

References 91 publications

Studies of Erk1/2 with Respect to Tumor Aggressiveness in B16f10 Murine Melanoma Cells

Studies of Erk1/2 with Respect to Tumor Aggressiveness in B16f10 Murine Melanoma Cells

Kaposi’s Sarcoma-Associated Herpesvirus ORF21 Enhances the Phosphorylation of MEK and the Infectivity of Progeny Virus

Kaposi’s Sarcoma-associated Herpesvirus ORF21 Enhances the Phosphorylation of MEK and the Infectivity of Progeny Virus

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