Special Issues

New Aspects of Noncoding RNAs in Cancer Proliferation and Metastasis

Submission Deadline: 30 April 2023 (closed) View: 9

Guest Editors

Dr. Shiyu Song; songshiyu@nju.edu.cn; Basic Medicine, Medical School of Nanjing University, Nanjing, China
Dr. Md Amir Hossain; E-mail: amir.hossain@monash.edu; Affiliation: Monash University, Australia
Dr. Junaid Wazir; E-mail: junaidwazir213@gmail.com; Affiliation: Nanjing University, China
Dr. Farhan Ullah Khan; E-mail: farhan.ullah.khan@usherbrooke.ca; Affiliation: University of Sherbrooke, Canada

Summary

Overproliferation is considered one of the most important hallmarks of cancer. In normal cells, cell division or the cell cycle are tightly regulated by multiple kinases and checkpoint inhibitors. In contrast, cancer cells acquire unlimited growth capacity, which is significantly related to worse treatment response and overall survival in various types of cancer patients. The enhanced proliferation not only compensated for the cell death induced either by anticancer drugs or immune cell attack but also forced the cancer cells to accumulate more mutations during DNA replication and chromatin reconstruction in the mitosis process.


Metastasis causes greater than 90% of cancer deaths. Unlike primary tumors, which can often be cured using local surgery, metastasis is much more difficult in clinical practice. In the past, metastasis was thought to occur at the late stage of cancer development. However, recent studies have indicated that the heterogeneity in tumor tissue shows that subsets of tumor cells in the tumor region acquire molecular features as metastatic cells in the relevant early stage. Thus, targeting potential metastasis should be considered a critical treatment strategy across all tumor stages.


There are close relationships and paradoxes between overgrowth and metastasis in different types of tumors. As mentioned above, cell division may result in the accumulation of metastasis-driving mutations in cancer cells and increase intratumor heterogeneity, resulting in more cancer stem cells or EMT cells. However, the original tumor has so-called distance suppression, which inhibits macrometastasis formation. Thus, the interaction between proliferation and metastasis should be thoroughly studied.


Approx. 75% of the human genome is transcribed into RNA, while only 3% is transcribed into protein-coding mRNAs. Thus, thousands of unique noncoding RNAs (ncRNAs) are synthesized and released by cells, either healthy or malignant. Several studies have shown that ncRNAs play crucial roles in both neoplastic and developing stages of cancer. They can work as oncogenes or suppressors to regulate cancer initiation and progression. Furthermore, secreted ncRNA will enhance the communication between tumor and normal cells, helping tumor cells shape a favorable tumor environment. Multiple studies have shown the regulatory effect of ncRNAs on both proliferation and metastasis in clinical and preclinical studies. Unlike proteins, ncRNAs, like miRNAs, target the mRNAs of many other genes involved in different biological processes. Thus, revealing the molecular function of ncRNA in both proliferation and metastasis might be critical for the treatment of cancer.


Here, we propose a special issue about new aspects of ncRNAs in cancer proliferation and metastasis. Original research and reviews are encouraged. Potential topics include but are not limited to the following:

1. Research on the clinical and basic aspects of the regulatory mechanism of long non-coding and microRNA on cell cycle in the cancer.

2. Research on the clinical and basic aspects of the regulatory function of long non-coding and microRNA on EMT in the cancer.

3. Using circulating non-coding RNA as biomarker for diagnosis and prognosis for cancer treatment.

4. The regulatory network of non-coding RNA in cancer stem cell formation.

5. The profile of exome of tumor cells and their contribution for tumor micro environment shaping.


Keywords

Proliferation; cell cycle; Metastasis; EMT; non-coding RNA; molecular biology; tumor microenvironment

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