Colorectal cancer (CRC) is one the leading causes of mortality related to cancer worldwide [[1], [2], [3]]. There are several treatment options for CRC, including surgery, targeted therapy, chemotherapy, immunotherapy, and radiotherapy [[4], [5], [6], [7], [8]]. Oxaliplatin (OXA) is one of the most common chemotherapeutic drugs used in CRC [[9], [10], [11]]. Unfortunately, resistance of CRC cells to OXA remains a critical obstacle to successful CRC treatment [12,13]. Therefore, identifying molecular mechanism underlying colorectal carcinogenesis is essential for the development of novel therapeutic targets against this debilitating disease [14].

Myeloblastosis viral oncogene homolog-like2 (B-MYB, alias of MYBL2), as a transcription factor of the myeloblastosis, regulates cell cycle progression, cell survival and cell differentiation of cancer cells [15]. B-MYB overexpression has been detected in a wide range of cancers, where it is associated with aggressive tumor growth and poor outcomes [16]. It is interesting to note that B-MYB is involved in the progression of CRC [17]. Also, the tumor-promoting role of B-MYB has been identified breast cancer resistance to tamoxifen [18]. Moreover, preliminary microarray analysis predicted a binding interaction between B-MYB and long noncoding RNA (lncRNA) colon cancer-associated transcript 1 (CCAT1). Importantly, CCAT1 has been documented to exhibit oncogenic effects in the development of CRC [19]. In addition, CCAT1 has been reported to accelerate the chemoresistance of colon cancer cells to paclitaxel by enhancing cell survival [20]. It is widely accepted that a number of lncRNAs can recruit DNA methyltransferase 1 (DNMT1), a process which alters the expression of downstream genes [21]. DNMT1 is upregulated in dysplastic cells, which is linked to low or absent suppressor of cytokine signaling 3 (SOCS3) expression [22]. Furthermore, the roles of SOCS3 in CRC development have also been demonstrated [23]. Given these findings, we sought to test the hypothesis that there might be a regulatory network of B-MYB, CCAT1, DNMT1, and SOCS3 that underpins the chemoresistance of CRC.