However, tamoxifen has no significant influence on CCNA2 expression in tamoxifen resistant subclones, which indicates CCNA2’s potential role in tamoxifen resistance. Nevertheless, whether CCNA2 is a driver gene in tamoxifen resistance still requires experimental validation. Provided the high expression of CCNA2 is involved in the development of tamoxifen resistance, how to manage cancer patients with CCNA2 overexpression remains a great challenge. Here we show several drugs that could influence the expression of CCNA2. For instance, Doxorubicin could decrease the expression of CCNA2, while Oxaliplatin could increase the expression of CCNA2. However, whether ER+ breast cancer patient with CCNA2 overexpression could benefit from the repression of CCNA2, or in other words, whether CCNA2 is a promising target for preventing or could reverse tamoxifen resistance still needs more experimental support. Although much information about ER and cancer has been provided in the past three decades since the arrival of tamoxifen in the clinic, a lot more needs to be elucidated for favorable therapeutic outcomes. More concrete research outcomes will warrant the translational research that may lead to more efficient and safer treatment for breast cancer patients as well as women at high risk of advanced breast cancer. Taken together, this study indicates that CCNA2 expression may help monitoring tamoxifen efficacy. In addition, it suggests the relevance of CCNA2 in the development of tamoxifen resistance. Furthermore, it could provide guidance personalized therapies. Nevertheless, multi-center randomized controlled clinical trials and in vivo/in vitro experiments are still needed before its application in clinical settings. Natural antisense transcripts, also called antisense RNAs, are RNAs that contain sequences that are complementary to other endogenous transcripts. Antisense RNAs may also encode proteins or may exist only as non-protein-coding transcripts. In recent years, investigations into NAT functions have indicated that NATs play key roles in carcinogenesis and the development of cancers. The tumor suppressor gene TP53 is the most frequently mutated gene in human cancers. P53 is a pivotal tumor suppressor that induces apoptosis, cell-cycle arrest, and senescence in response to stress signals such as DNA damage, hypoxia, or activated oncogenes. A natural antisense transcript to p53 has recently been identified; WRAP53 gives rise to p53 antisense transcripts that regulate p53 mRNA expression and are required for p53 activity upon DNA damage. WRAP53 transcripts may also be translated into WRAP53 protein, supporting the proliferation of progenitor cells and tumor cells by binding to telomerase to add telomere repeats to Danshensu chromosome ends. Esophageal cancer is one of the most common malignant tumors, resulting in poor prognosis worldwide. ESCC is the most frequent histological EC subtype, accounts for more than 90% of ECs, and results in clinical outcomes with high mortality rates in China. Esophageal carcinogenesis involves multiple cellular alterations, including Echinacoside aberrant cell cycle control, DNA repair, cellular enzymes, and growth factor and nuclear receptors.