Heterochromatin Protein 1α: A Characteristic of Cell Proliferation That is Pertinent to Clinical Oncology

Wenbin Lin^*
*Correspondence: Wenbin Lin, Department of Chemistry, University of Chicago, Chicago, USA, Email:

Keywords

Heterochromatin • Tumorigenesis • Clinical oncology

Introduction

For a considerable amount of time, it has been assumed that cancer is a genetic condition brought on primarily by mutations in DNA sequences, either naturally occurring or inherited. However, chromatin organization changes have recently been linked to tumorigenesis as well, and extensive research has been done to learn how these processes interact with one another. The characterization of changes in DNA methylation and various histone modifications has required significant effort. With some success, drugs that target these modifications have begun to be used in cancer treatment. A current test is to track down how, past DNA and histones, the higher request atomic association of chromatin, which is many times impacted in disease cells, partakes in tumourigenesis. In this regard, breast cancer is a particularly intriguing model. It cannot be explained as a genetic disease because of its clinical and genetic heterogeneity. As a result, it is particularly important to consider whether breast cancer cells exhibit particular chromatin modifications that may encourage tumorigenesis to proceed. The observation that HP1 interacts with the tumor suppressor Retinoblastoma protein (Rb) and participates in the Rb-dependent silencing of cell cycle genes like Cyclin E provided the first possible link between HP1 proteins and tumorigenesis. The transcriptional co-repressor KAP-1, which is involved in the regulation of the E2F1 and p53 proteins, also interacts with HP1.

Literature Review

In addition, HP1 and have been found to be in complex with Chromatin assembly factor 1, of which the intermediate subunit p60 has been demonstrated to be a breast cancer-specific proliferation marker. We considered the regulation of the various HP1 isoforms in relation to cell proliferation and tumorigenesis as a result of these arguments. Interestingly, the HP1 promoter region contains potential E2F protein and myc transcription factor target sites. Furthermore, when compared to their undifferentiated precursors, all three HP1 isoforms are downregulated in differentiated blood lymphocytes. It has not been determined whether this downregulation is a general response to cell cycle exit or a specific characteristic of blood cell differentiation. Breast cancer cells with lower levels of HP1 have also been found to have a greater capacity for invasiveness; however, it is still not clear to which aspect of the metastasis process this downregulation pertains. As a result, it is still unclear what regulation patterns the three HP1 isoforms share with regard to cell proliferation, quiescence, and cancer. Using both human cell line models and a collection of human tumor-derived tissue samples, we decided to conduct a comprehensive study of the behavior of the various HP1 isoforms during cell proliferation, cell cycle exit, and tumorigenesis to resolve these issues [1,2].

Discussion

A proliferation-dependent expression pattern is a novel feature of HP1 that we demonstrate. Upon transient cell cycle leave, the outflow of HP1α, yet not β or γ, is diminished. When compared to non-tumoral mammary cells from the same patient, breast cancer cell lines overexpress HP1 but not. Surprisingly, HP1 is overexpressed in non-tumoral tissues of the pancreas, uterus, ovary, breast, and prostate cancers, as well as in uterine leiomyoma. In addition, there is a strong correlation between the occurrence of metastasis and the progression of the disease in breast carcinomas that have been followed for a considerable amount of time. According to our findings, there is a clear link between HP1 levels and cell proliferation, which is important for determining the tumorigenicity and prognosis of breast cancer. Overexpressed HP1 in tumoral cells may play a role in chromatin organization, according to our analysis of the chromatin-bound and soluble fractions [3,4].

This suggests that HP1 is partially bound to the chromatin. This is by all accounts reliable with its atomic restriction, which is granular and diffuse in the non-tumoural mammary cells however obviously confined into discrete spots in a huge part of the bosom disease cells. The autoimmune serum CREST found these spots mostly in centromeric areas. However, the different patterns of HP1 staining do not appear to be associated with specific stages of the cell cycle, as demonstrated by staining for cell cycle markers (Fig S4C in Supporting Information), and the various forms of localization of HP1 were not accompanied by an altered nuclear distribution of H3K9me. All in all, our cell line model shows an overexpression of HP1α, however not HP1β or γ, in tumoural mammary cells contrasted with non-tumoural mammary cells. In breast cancer cells, a significant amount of HP1 is chromatin-bound and localizes to centromeric regions. In the past, several breast cancer cell lines decreased invasive potential was correlated with an increase in HP1 expression, possibly through the suppression of pro-invasive genes. In fact, metastasis necessitates the acquisition of invasive potential and the adaptation to a new environment, both of which are frequently incompatible with high proliferation rates, so this observation may reflect the inverse correlation that has been suggested between invasion and proliferation [5,6].

Conclusion

Consequently, a transient log jam of growth expansion, joined by down regulation of HP1α, could allow the statement of supportive of intrusive qualities and the event of metastasis. However, because high HP1 expression was correlated with an earlier diagnosis of metastasis, our data suggest that cell proliferation is the most important process for final patient outcome in the outgrowth of metastases.

Acknowledgement

None.

Conflict of Interest

No potential conflict of interest was reported by the authors.

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