Higher Expression of the Heterogeneous Nuclear Ribonucleoprotein K in Melanoma

Wen, Fushi; Shen, Alex; Shanas, Reneé; Bhattacharyya, Achyut K.; Lian, Fangru; Hostetter, Galen; Shi, Jiaqi

doi:10.1245/s10434-010-1121-1

Cited by 42 publications

(44 citation statements)

References 34 publications

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“…These studies revealed that increased hnRNP K expression associated with poor clinical status in melanoma, prostate, breast, lung, colorectal, hepatocellular, and esophageal cancers. [14][15][16][17][18] Given the myriad of tumor types that overexpress hnRNP K in these studies and its correlation with disease prognosis, these data suggest that hnRNP K may have oncogenic functions when overexpressed.…”

Section: Clinical Evidence For a Role Of Aberrant Hnrnp K In Tumorigementioning

confidence: 75%

“…[14][15][16][17][18] However, to directly test this notion, there is an absolute need for the development of transgenic animal models that overexpress wild-type hnRNP K. We have currently undertaken this task by generating tissuespecific Hnrnpk transgenic mice. These model systems will directly test whether hnRNP K is a bona fide oncogene and will be useful in identifying the genes and cellular programs critical for tumorigenesis when hnRNP K is overexpressed.…”

Section: Summary and Future Directionsmentioning

confidence: 99%

“…[8][9][10][11][12][13] In support of its potential oncogenic functions, clinical association studies suggest that hnRNP K overexpression correlates with poor clinical outcomes and advanced disease status in a variety of malignancies, including melanoma, prostate, breast, lung, colorectal, hepatocellular, and esophageal cancers. [14][15][16][17][18] In contrast, other clinical studies suggest reduced hnRNP K expression, due to deletion of or mutations in the HNRNPK gene, may underpin the pathogenesis of acute myeloid leukemia (AML). [19][20][21][22][23] In the case of mutation, there are further questions concerning whether specific mutations inactivate the protein or potentially stabilize or confer gain-of-function phenotypes, reminiscent of mutations observed in the c-Myc protein and mutant p53 proteins, respectively.…”

Section: Introductionmentioning

confidence: 99%

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Aberrant hnRNP K expression: All roads lead to cancer

et al. 2016

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The classification of a gene as an oncogene or a tumor suppressor has been a staple of cancer biology for decades. However, as we delve deeper into the biology of these genes, this simple classification has become increasingly difficult for some. In the case of heterogeneous nuclear ribonuclear protein K (hnRNP K), its role as a tumor suppressor has recently been described in acute myeloid leukemia and demonstrated in a haploinsufficient mouse model. In contrast, data from other clinical correlation studies suggest that hnRNP K may be more fittingly described as an oncogene, due to its increased levels in a variety of malignancies. hnRNP K is a multifunctional protein that can regulate both oncogenic and tumor suppressive pathways through a bevy of chromatin-, DNA-, RNA-, and protein-mediated activates, suggesting its aberrant expression may have broad-reaching cellular impacts. In this review, we highlight our current understanding of hnRNP K, with particular emphasis on its apparently dichotomous roles in tumorigenesis.

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Section: Clinical Evidence For a Role Of Aberrant Hnrnp K In Tumorigementioning

confidence: 75%

Section: Summary and Future Directionsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Aberrant hnRNP K expression: All roads lead to cancer

et al. 2016

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“…hnRNPs include at least 20 discrete hnRNPs that are labeled as hnRNP A through U. These hnRNPs are actively involved in many facets of mRNA metabolism, from transcription to post-transcriptional events and translation (Papadopoulou et al, 2013;Wen et al, 2010). ELAV is another important small family of RBPs that comprises four members: HuR, HuB, HuC, and HuD.…”

Section: Discussionmentioning

confidence: 99%

Lipoteichoic Acid Isolated from Lactobacillus plantarum Inhibits Melanogenesis in B16F10 Mouse Melanoma Cells

Kim¹,

Kim²,

Jung³

et al. 2015

Molecules and Cells

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Lipoteichoic acid (LTA) is a major component of the cell wall of Gram-positive bacteria. Its effects on living organisms are different from those of lipopolysaccharide (LPS) found in Gram-negative bacteria. LTA contributes to immune regulatory effects including anti-aging. In this study, we showed that LTA isolated from Lactobacillus plantarum (pLTA) inhibited melanogenesis in B16F10 mouse melanoma cells. pLTA reduced the cellular activity of tyrosinase and the expression of tyrosinase family members in a dose-dependent manner. The expression of microphthalmia-associated transcription factor (MITF), a key factor in the synthesis of melanin, was also decreased by pLTA. Further, we showed that pLTA activated melanogenesis signaling, such as extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3-kinse (PI3K)/AKT. In addition, the expression of heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) and HuR, which are important RNA-binding proteins (RBPs), was reduced. pLTA likely degrades MITF via regulation of melanogenic signaling and RNA stability of melanogenic proteins, resulting in the reduction of melanin. Thus, our data suggest that pLTA has therapeutic potential for treating hyperpigmentation disorders and can also be used as a cosmetic whitening agent.

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“…hnRNP K participates in the regulation of various physiological and pathological processes, including development [18–22], DNA damage response [23] and several human diseases [24–29]. It was reported recently that hnRNP K mRNA was gradually decreased in the rat central nervous system, but remained high in the peripheral nervous system throughout embryonic development [22].…”

Section: Introductionmentioning

confidence: 99%

Transcriptional regulation of heterogeneous nuclear ribonucleoprotein K gene expression

Xue

Wang

et al. 2015

Biochimie

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Heterogeneous nuclear ribonucleoprotein K (hnRNP K) is importantly involved in the regulation of development, DNA damage response, and several human diseases. The molecular mechanisms that control the expression of hnRNP K are largely unknown. In the present study, we investigated the detailed mechanism of the transcriptional regulation of human hnRNP K gene. Two activating and one repressive elements located in the proximal segment of the transcriptional initiation site were identified in hnRNP K gene. A 19 bp-region was responsible for the inhibitory activities of the repressor element. Twenty proteins were identified by DNA-affinity purification and mass spectrometry analyses as binding partners of the primary activating element in the hnRNP K promoter. Chromatin immunoprecipitation and EMSA analysis confirmed the binding of Sp1 with hnRNP K promoter. Sp1 enhanced the promoter activity, increased the expression of hnRNP K, and reduced the mRNA level of angiotensinogen, a gene known to be negatively regulated by hnRNP K. In summary, the current study characterized the promoter elements that regulate the transcription of human hnRNP K gene, identified 20 proteins that bind to the primary activating element of hnRNP K promoter, and demonstrated a functional effect of Sp1 on hnRNP K transcription.

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Higher Expression of the Heterogeneous Nuclear Ribonucleoprotein K in Melanoma

Cited by 42 publications

References 34 publications

Aberrant hnRNP K expression: All roads lead to cancer

Aberrant hnRNP K expression: All roads lead to cancer

Lipoteichoic Acid Isolated from Lactobacillus plantarum Inhibits Melanogenesis in B16F10 Mouse Melanoma Cells

Transcriptional regulation of heterogeneous nuclear ribonucleoprotein K gene expression

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